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Saturday, December 29, 2007
References
Two MSCs
Conclusion
Mesenchymal stem cells can be isolated from bone marrow by standardized techniques and expanded in culture through many generations, while retaining their capacity to differentiate along set pathways when exposed to appropriate conditions. This property opens up therapeutic opportunities for the treatment of lesions in mesenchymal tissues, and protocols have been devised for the treatment of defects in articular cartilage 71), bone 72), tendon 73), and meniscus 74) and for bone marrow stromal recovery 75) and osteogenesis imperfecta 76).
In this context, we prefer to use the word ‘stroma’ rather than ‘mesenchymal stem cells’ for accuracy and to avoid confusion. In the field of hematopoiesis, marrow stroma were originally treated as ‘second class citizens’ 77), and represented a niche field. Today, marrow stroma are a ‘major player’ in regenerative medicine and stem cell biology and are no longer viewed as a peripheral field of research. In addition, there is also a rapidly growing body of research into the biology and potential use of true ‘mesenchymal stem cells’ derived from other human tissues, which are showing significant promise for future therapy, reparation or regeneration of human tissues and organs.
Clearly, this field is in its relative infancy, our understanding is at present limited but the potential benefits are great. We should perhaps, therefore, remember that the unexpected and unrivalled potential of MSCs to differentiate into a wide variety of cells represents a gift not a privilege and, with respect to the two MSCs, we should recognise and welcome their role in medicine with the words “with great power comes great responsibility”.
Differentiation of mesenchymal stem cells
Fig. 3. Model of stem cell differentiation.
A.Deterministic model.
B.Stochastic model.
C.Differentiation model of mesenchymal stem cells.
Retroviral labeling of individual cells is a useful clonal assay to monitor lineage commitment at the single cell level. At present, several models have been proposed in which hematopoietic lineage determination is driven intrinsically 68), extrinsically 69), or both 70). The issue of the mechanism and the extent of cellular differentiation that occurs when stem cells begin to differentiate is the area of furthest advanced research. Two models have been proposed: a deterministic model, in which differentiation is governed by the microenvironment (including growth factors and cytokines), and a stochastic model, in which differentiation, self-replication and the direction of differentiation emerge somewhat randomly (Fig. 3A, B). The different models arise from different conceptions of mesenchymal stem cells. The mesenchymal stem cell (MSC2) line is stochastically committed toward the cardiac lineage, and following this commitment, they proliferate as transient amplifying cells and differentiate into cardiac myocytes (Fig. 3C).
Considering stem cell transplant as a therapy, when mature cells arising from hematopoietic stem cells are needed, as in marrow transplant, there are no problems attending cellular differentiation. However, in the case of cells that serve to originate cells of several different organs, as in the case of mesenchymal stem cells, there is a possibility for differentiation to cells not needed in the treatment. Ectopic tissue may therefore emerge from implanted mesenchymal stem cells, especially where the buffering system from a given site is lost and the stem cells begin to differentiate randomly into cells differing from the implanted site, thereby creating unwanted ectopic tissue.
Life span of MSC1 and MSC2.
Marrow stromal cells (MSC1) and mesenchymal stem cells (MSC2) are useful for cell transplantation. However, it is difficult to study and apply them because of their limited life span. One of the reasons for this is that normal human cells undergo a limited number of cell divisions in culture and then enter a non-dividing state called “senescence” 62, 63). Human cells reach senescence after a limited number of cell replications, and the average number of population doublings (PDs) of marrow-derived mesenchymal stem cells has been found to be about 40 42), implying that it would be difficult to obtain enough cells to restore the function of a failing human organ. Large numbers of cells must be injected into damaged tissues to restore function in humans, and cells sometimes need to be injected throughout entire organs.
A system that allows human cells to escape senescence by using cell-cycle-associated molecules may be used to obtain sources of material for cell therapy 64, 65). Both inactivation of the Rb/p16INK4a pathway and activation of telomerase are required for immortalization of human epithelial cells, such as mammary epithelial cells and skin keratinocytes. Human papillomavirus E7 can inactivate pRb, and Bmi-1 can repress p16INK4a expression. Inactivation of the p53 pathway is also beneficial, even if not essential, to extension of the life span 66). Human marrow stromal cell strains with an extended life span can be generated by transduction of combination of TERT, and Bmi-1, E6 or E7 45). Cells with extended life span grow in vitro for over 80 PDs, and their differentiation potential is maintained. Transfection of TERT alone is insufficient to prolong the life span of marrow stromal cells, despite TERT having been reported to extend the life span of cells beyond senescence without affecting their differentiation ability 67). Human stromal cells transfected with TERT and Bmi-1, E6 or E7 do not transform according to the classical pattern: they do not generate tumors in immunosuppressed mice; they do not form foci in vitro; and they stop dividing after confluence. The possibility that gene-transduced stromal cells might become tumorigenic in patients several decades after cell therapy therefore cannot be ruled out. Nevertheless, these gene-modified stromal cells may be used to supply defective enzymes to patients with genetic metabolic diseases, such as neuro-Gaucher disease, Fabry disease, and mucopolysaccharidosis, which have a poor prognosis and are sometimes lethal. The 'risk versus benefit' balance is essential when applying these gene-modified cells clinically, and the 'risk' or 'drawback' in this case is transformation of implanted cells. These marrow stromal cells (MSC1) with prolonged life span also provide a novel model for further study of cancer and stem cell biology.
Available mesenchymal cell lines and mesenchymal cells in culture
Fig. 2. Sources and differentiation of mesenchymal stem cells.
MSC2 have been extracted from fat, muscle, menstrual blood, endometrium, placenta, umbilical cord, cord blood, skin, and eye (Fig. 2). Moreover, the source tissues can be obtained without difficulty from resected tissues at surgery and from birth deliveries (http://www.nch.go.jp/reproduction/cellbank2.htm and http://www.nch.go.jp/reproduction/cells/primary.html); menstrual blood can be provided from volunteers. The placenta is composed of amniotic membrane, chorionic villi and decidua, each of which can be a source of different types of MSC2. Large numbers of MSC2 can be easily obtained because the placenta is usually provided for research purposes. Menstrual blood also contains a large number of MSC2, although it is usually regarded as waste material.
We have also isolated many specific cell lines from adhering cells of mouse bone marrow (http://www.nch.go.jp/reproduction/cellbank2.htm) as follows:
a.Multi-potential stem cell line: 9-15c cells (originally KUM2 cells) have multi-potential allowing differentiation into bone, fat, skeletal muscle, and myocardial cells through continued passage;
b.Oligo-potential cell lines: KUM9 cells that lose the ability to differentiate to myocardial cells but retain differentiation to bone, fat, and skeletal muscle and NRG cells that lose the capability to differentiate into myocardial cells and skeletal myocytes but retain differentiation to bone and fat;
c.Bi-potential cells: KUSA-O cells are capable of differentiating into osteoblasts and adiopocytes;
d.Precursor cells: KUSA-A1 and H-1/A are osteoblasts and preadipocytes, respectively. Adipogenic 3T3-L1 56), osteogenic MC3T3-E1 57), and chondrogenic ATDC5 cells 58) have been isolated from stem cells of a mesenchymal nature.
Focusing on human MSC2 derived from umbilical cord blood (UCBMSC) as an example, isolation, characterization, and differentiation of clonally-expanded UCBMSCs have been reported 59, 60), and UCBMSCs have been found to have multi-potential 61). Most of the surface markers are the same as those detected in their bone marrow counterparts 42), with both UCB- and bone marrow-derived cells being positive for CD29, CD44, CD55, and CD59, and negative for CD34 and CD117. Significantly, the differentiation capacity of UCB-derived cells is unaffected during establishment of a plate-adhering population of cells from UCB.
Mesenchymal stem cells (MSC2)
Tissues originating in the mesoderm include blood cells, blood vessels, heart, bone, cartilage, fat, skeletal muscle, tendon, and tissue mesenchyme. Blood cells in bone marrow are the elements that create the concept of stem cells, but bone marrow includes another cell group, i.e., mesenchymal stem cells (MSC2), which possess adherent properties. These cells have the ability to differentiate into a variety of cells and may have an organ maintenance mechanism that serves as back-up. Human mesenchymal stem cells (MSC2) are a useful source of cells for transplantation for several reasons: they have the ability to proliferate and differentiate into mesodermal tissues and they entail no ethical or immunological problems. MSC2 have been studied extensively over the past three decades and numerous independent research groups have successfully isolated them from a variety of sources, most commonly from bone marrow 19, 22, 52-55). Yet, in addition to bone marrow, almost all human tissues or organs can be a source of mesenchymal stem cells, since they all have stroma or mesenchyme as well as parenchyma or epithelium.
Epigenetic modifier as a differentiating inducer.
The demethylating agent, 5-azacytidine, is a cytosine analog that has a remarkable effect on transdifferentiation of cells and has been shown to induce differentiation of mesenchymal cells into cardiomyocytes, skeletal myocytes, adipocytes, and chondrocytes 19, 42, 47). The effect of this low-molecular substance is not surprising, since it is incorporated into DNA and has been shown to cause extensive demethylation. The demethylation is attributable to covalent binding of DNA methyltransferase to 5-azacytidine in the DNA 48), with subsequent reduction of enzyme activity in cells resulting in dilution-out and random loss of methylation at many sites in the genome. This may, in turn, account for the reactivation of cardiomyogenic ‘master’ genes, such as MEF-2C, GATA4, dHAND, and Csx/Nkx2.5, leading to stochastic transdifferentiation of MSC1 into cardiomyocytes. Use of 5-azacytidine is beneficial, but since it may have drawbacks, i.e., gene activation leading to oncogenesis and undesired differentiation, care must be exercised before using it to induce cells to differentiate into target phenotypes. Immortalized cells, including marrow stromal cells, have specific patterns of DNA methylation. The established methylation pattern of cells is maintained with considerable fidelity and silenced genes are stably inherited throughout the culture period 49-51). The demethylating agent induces differentiation by altering the original methylated pattern and reactivating the silenced genes.
Cardiomyogenesis and Neurogenesis
3) Cardiomyogenesis
It has been generally accepted that cardiac myocytes are unable to divide once cell proliferation ceases shortly after birth in the mammalian heart, because mitotic figures have not been detected in myocytes 38). Cardiomyocytes induce DNA synthesis in vivo and in vitro 39, 40). Adult hearts often exhibit a polypoid structure, which results from stochastic accumulation of mutations as cells pass through cell-cycle checkpoints 41). Bone marrow-derived stromal cells (MSC1) are able to differentiate into cardiomyocytes in vitro and in vivo 19, 20, 42, 43) and a hierarchical model has been proposed for this in vitro cardiomyogenic differentiation. MSC1 in culture include a mixture of at least three types of cells, i.e., cardiac myoblasts, cardiac progenitors and multi-potential stem cells, and a follow-up study of individual cells suggests that commitment of a single-cell-derived stem cell toward a cardiac lineage is stochastic 44). Furthermore, MSC1 over-expressing well-known master transcription factors, i.e., Csx/Nkx2.5 and GATA4, unavoidably undergo cardiomyogenic fate and behave like transient amplifying cells. MSC1 also transdifferentiate into cardiomyocytes in response to humoral factors, such as demethylation of the genome, in addition to environmental factors (See the chapter “Epigenetic modifier as a differentiating inducer”.
4) Neurogenesis
MSC1 can exhibit neural differentiation when exposed to demethylating agents 14): the cells differentiating into three types of neural cells, i.e., neurons, astrocytes, and oligodendrocytes. With exposure to basic fibroblast growth factor, nerve growth factor, and brain-derived neurotrophic factor, the transdifferentiation of human stromal cells is limited to neurons 14). The change in gene expression during differentiation is global and drastic 45): the differentiated cells no longer exhibit the profile of mesenchymal cells or the biphenotypic pattern of neuronal and mesenchymal cells. Osteoblasts capable of intra-membranous ossification are likely to differentiate into neuronal lineages, but adipocytes do not 14). Interestingly, the cranio-facial membranous bones develop from the neural crest, which is of ectodermal origin. Development naturally progresses from neural crest cells to terminally-differentiated osteoblasts 46). The finding of in vitro differentiation from mesoderm- to ectoderm-derived cells is thus the opposite of the developmental process, i.e., from ectoderm- to mesoderm-derived cells. Converting differentiated osteoblasts or MSC1 to neuronal cells, a key future task for any cell-based therapy, would thus oppose the usual direction of cell differentiation. This can now be achieved by exposing stromal cells to neurotrophic factors, at least in vitro.
Dopaminergic neuron-associated genes, such as nurr1 and wnt-5a, are induced at an extremely high level in the neuronally-differentiated stromal cells. Wnt5a and nurr1 are involved in the differentiation of mid-brain precursors into dopaminergic neurons 25, 26). It is quite significant that dopaminergic neurons can be generated from MSC1, since they are one of the key targets for regenerative medicine.
Osteogenesis and chondrogenesis of bone marrow stromal cells
Bone marrow stromal cells (MSC1)
The existence of non-hematopoietic cells in bone marrow was first suggested by Cohnheim about 130 years ago 16). Bone marrow-derived stromal cells (MSC1) can differentiate into most somatic cells, including osteoblasts, chondrocytes, myoblasts, cardiomyocytes 17-21), and adipocytes, when placed in appropriate in vitro 20) and in vivo environments 22), and thus are a useful cell source for regenerative medicine 23). Recent studies suggest that MSC1 can also differentiate into a neuronal lineage 24), and murine bone marrow-derived adult progenitor cells can differentiate into dopaminergic neuronal cells 25, 26). Since the use of MSC1 entails no ethical or immunological problems, and bone marrow aspiration is an established routine procedure, these cells provide a useful and almost routine source of material for transplantation and tissue repair or regeneration (Fig. 1: http://blogs.yahoo.co.jp/akihiroumezawa/19883767.html).
1) Osteogenesis
KUSA-A1 cells, a murine marrow stromal cell line, are capable of generating mature bone in vivo 27). They are a unique, mature osteoblast cell line and serve as a very suitable model for in vivo osteogenesis. Bone forms in subcutaneous tissue after subcutaneous injection of the cells into mice. The osteogenesis by KUSA-A1 is not mediated by chondrogenesis and thus is considered to be membranous ossification. Follow-up study on the fate of bone by immortalized osteoblasts shows that the ectopically-generated bone keeps its size and shape for 12 months 21). Furthermore, the implanted cells do not metastasize like tumor cells. These unique characteristics of KUSA-A1 cells provide an opportunity to analyze the process of membranous ossification in detail.
2) Chondrogenesis
Chondrocytes differentiate from mesenchymal cells during embryonic development 28) and the phenotype of the differentiated chondrocyte is characterized by the synthesis, deposition, and maintenance of cartilage-specific extracellular matrix molecules, including type II collagen and aggrecan 29-31). The phenotype of differentiated chondrocytes is rapidly lost since it is unstable in culture 32-35). This process is referred to as 'dedifferentiation' and is a major impediment to use of mass cell populations for therapy or tissue engineering of damaged cartilage. When isolated chondrocytes are cultured in a monolayer at low density, the typical round chondrocytes morphologically transform into flattened fibroblast-like cells, with profound changes in biochemical and genetic characteristics, including reduced synthesis of type II collagen and cartilage proteins 36). When cultured three-dimensionally in a scaffold such as agarose, collagen, and alginate, redifferentiated chondrocytes re-express the chondrocytic differentiation phenotype.
KUM5 mesenchymal cells, a MSC1 line, generate hyaline cartilage in vivo and exhibit endochondral ossification at a later stage after implantation 37). OP9 cells, another MSC1 line, derived from macrophage colony-stimulating factor-deficient osteopetrotic mice, and also known to be niche-constituting cells for hematopoietic stem cells, express chondrocyte-specific or -associated genes, such as type II collagen 1, Sox9, and cartilage oligomeric matrix protein at an extremely high level, as do KUM5 cells. OP9 micromasses exposed to TGF- 3 and BMP2 form type II collagen-positive hyaline cartilage within two weeks in vivo. The unique characteristics of KUM5 and OP9 cells provide an opportunity to analyze the process of endochondral ossification.
Two MSCs: Marrow stromal cells and mesenchymal stem cells---Introduction---
Fig. 1. Development and differentiation of mesenchymal stem cells derived from bone marrow.
Introduction
Two MSCs, i.e., marrow stromal cells (MSC1) and mesenchymal stem cells (MSC2), are attracting a great deal of attention, as they represent a valuable source of cells for use in regenerative medicine, as well as offering an excellent model of cell differentiaton in biology. However, confusion exists in the literature due to poor application or misuse of the terms and nomenclature.
In general, mesenchymal stem cells are multi-potential stem cells that can differentiate into a variety of cell types (ref. http://en.wikipedia.org/wiki/Mesenchymal_stem_cell). They have been shown to differentiate, in vitro or in vivo, into osteoblasts, chondrocytes, myocytes, adipocytes and neuronal cell among others. Mesenchymal stem cells have traditionally been obtained from bone marrow, and have commonly been referred to as ‘marrow stromal cells’ (MSC1).
While the terms ‘marrow stromal cell’ (or ‘stromal cell’) and ‘mesenchymal stem cell’ have frequently been used interchangeably, they are increasingly recognized as separate entities as:
1. Stromal cells (MSC1) are a highly-heterogenous cell population, usually derived from bone marrow, consisting of multiple cell types with different potentials for proliferation and differentiation.
2. Mesenchymal stem cells (MSC2) encompass cells derived from other non-marrow tissues, such as fat, muscle, menstrual blood, endometrium, placenta, umbilical cord, cord blood, skin, and eye.
Bone marrow-derived mesenchymal stem cells or bone marrow stromal cells (MSC1) were discovered by Friedenstein in 1976, who described clonal, plastic-adherent cells from bone marrow that were capable of differentiating into osteoblasts, adipocytes, and chondrocytes. More recently, investigators have demonstrated that mesenchymal stem cells (MSC2) per se can be recovered from a variety of adult tissues and have the capacity to differentiate into a variety of specialist cell types. This review describes the recent advances in understanding of the two MSC cells, their biology and ongoing investigation and use.
Thursday, November 29, 2007
Two MSCs: Marrow stromal cells and mesenchymal stem cells
Two MSCs: Marrow stromal cells and mesenchymal stem cells
Marrow stromal cells are able to generate a series of terminally differentiated cells in vitro. However, most of these experiments are performed with heterogeneous stromal cells, which had been obtained by adherence to plastic culture dishes. Since it is demonstrated that bone marrow-derived stromal cells are purified to a homogeneous population that met the criteria for nonhematopoietic stem cells, these cells have been termed mesenchymal stem cells because they generate an array of cells, defined as mesenchymal cells. In contrast, mesenchymal stem cells are multipotent cells capable of differentiating into cells of mesoderm-origin regardless of cell sources. Mesenchymal stem cells can be recovered from a variety of other adult tissues such as fat, muscle, menstrual blood, endometrium, placenta, umbilical cord, cord blood, skin, and eye. The terms mesenchymal stem cell and stromal cell, both of which are most plausible cells for regenerative medicine, have been used interchangeably in emerging literature; we here re-organize our understanding on two MSC biology and further clinical trail in this review.
Introduction
http://blogs.yahoo.co.jp/akihiroumezawa/19883767.html
Friday, November 23, 2007
Shortening of human cell life span by platelet-derived growth factor via induction of p16ink4a
Shortening of human cell life span by platelet-derived growth factor via induction of p16ink4a
Cells vary in their requirements in a cell type-specific manner, and cells can therefore be categorized or defined by their requirements. In this study, we attempted to prolong life span of a marrow-derived mesenchymal stem cell using a combination of growth factors and hormones. Epidermal growth factor, platelet-derived growth factor-BB, acidic fibroblast growth factor (FGF), basic FGF, and leukemia inhibitory factor were found to be key factors for the mesenchymal stem cell proliferation. The combination of these growth factors showed extremely strong mitogenic activity, and simultaneously induced the expression of cyclin-dependent kinase inhibitor p16ink4a protein and premature senescence more rapidly than serum-supported culture conditions. The induction of p16ink4a by growth factors was mediated through the mitogen-activated protein kinase (MAPK) cascade. Excess growth stimulation by growth factors was thus one of the culture stress signals and a trigger of premature senescence at least in human cells.
Wednesday, November 21, 2007
Supporting materials
Isolation and cell culture of human mesenchymal stem cells.
After obtaining signed informed consent, mesenchymal stem cells and mesenchymal cells were harvested from human donors with the approval of the Ethics Committee of Keio University School of Medicine (approval number: 13-1 and 12-1) and the Ethics Committee of National Research Institute for Child Health and Development, Tokyo (approval number: 25, 26, 27, 49, 55, 88, 89, 90, 91, 146, and 156). Cells were resuspended in growth medium (the M061101 medium, MED SHIROTORI Co., Ltd., Tokyo; MSCGM, PT-3238 and PT-4105, Cambrex Bio Science Walkersville, inc. Walkersville, MD) and cultured as previously described (1-3). Cells were deposited to the RIKEN CELL BANK (http://www.brc.riken.go.jp/lab/cell/english/guide.shtml) and the Health Science Research Resources Bank (http://www.jhsf.or.jp/English/index_gc.html).
G-banding karyotypic analysis and spectral karyotyping (SKY) analysis.
We performed a karyotypic analysis (G-banding and SKY) of both the mesenchymal stem cells and mesenchymal cells (Fig. 1, 2. A: Yub10F; B: Yub623; C: Yub625; D: Yub627; E: UCB302; F: UCB408; G: UCB432; H: PL502; I: PL503; J: PL504; K: PL505; L: PL506; M, N: PL507). Metaphase spreads were prepared from at least 50 cells treated with Colcemid (Karyo Max, Gibco Co. BRL, 100 ng/ml for 6 hours). We performed a standard G-banding karyotypic analysis on metaphase spreads for each population. SKY permits a detailed analysis of all complex markers and provides insights into their involvement in subsequent rearrangements (4). No genomic abnormalities were found in the cells analysed as shown by G-banding (Fig. 1) and SKY analysis (Fig. 2).
Cell transplantation and in vivo tumor formation assay
Freshly collected confluent cells (106 cells) were subcutaneously and intramuscularly injected into Balb/c nu/nu mice (Sankyo Laboratory, Hamamatsu, Japan) and NOD/SCID/IL-2 receptor common gamma knockout (NOG) mice. Animals were monitored for malignant transformation of the injected cells after inoculation and then sacrificed by cervical location. Nor did the cells grafted into the subcutaneous and muscle tissue of nude mice and NOG mice produce tumors. Furthermore, the cells did not undergo malignant transformation in vitro: They stopped dividing after reaching confluence, and they did not form any foci after confluence in vitro.
Telomerase activity and telomere length in human mesenchymal stem cells.
Telomerase activity was determined with a TRAP assay kit “Telo TAGGG telomerase PCR ELISA plus” (Roche, Indianapolis, IN) according to the manufacturer’s instructions. No telomerase activity was detected by the TRAP assay in the mesenchymal stem cells and mesenchymal cells. For the telomere length assay, genomic DNA was extracted from cultured cells. Restriction enzyme digestion of genomic DNA was carried out with Hinf I and Rsa l. The fragments obtained were resolved on 0.7% agarose gels, transferred to a Hybond N membrane (Amersham, UK), and hybridized with digoxigenin (DIG)-labeled (TTAGGG)3 probe. The membrane was then incubated with anti-DIG alkaline phosphatase and detection was performed with a chemiluminescence solution. The size range and intensity were determined with X-ray film. The telomere length of the mesenchymal stem cells and mesenchymal cells decreased with the number of PDs.
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2. Imabayashi, H., T. Mori, S. Gojo, T. Kiyono, T. Sugiyama, R. Irie, T. Isogai, J. Hata, Y. Toyama, and A. Umezawa, Redifferentiation of dedifferentiated chondrocytes and chondrogenesis of human bone marrow stromal cells via chondrosphere formation with expression profiling by large-scale cDNA analysis. Exp Cell Res, 288: 35-50, 2003.
3. Terai, M., T. Uyama, T. Sugiki, X.K. Li, A. Umezawa, and T. Kiyono, Immortalization of Human Fetal Cells: The Life Span of Umbilical Cord Blood-derived Cells Can Be Prolonged without Manipulating p16INK4a/RB Braking Pathway. Mol Biol Cell, 16: 1491-1499, 2005.
4. Schrock, E., T. Veldman, H. Padilla-Nash, Y. Ning, J. Spurbeck, S. Jalal, L.G. Shaffer, P. Papenhausen, C. Kozma, M.C. Phelan, E. Kjeldsen, S.A. Schonberg, P. O'Brien, L. Biesecker, S. du Manoir, and T. Ried, Spectral karyotyping refines cytogenetic diagnostics of constitutional chromosomal abnormalities. Hum Genet, 101: 255-62, 1997.
Can a human adult stem cell spontaneously transform?
ãã现èã«é¢ãã、å¹é€éçšã§ã®çåã®å¯èœæ§ã«ã€ããŠèšåããŸãã。äžã®æç« ã«ã¯、å€å°ééã（æè²äœç°åžžã®åºçŸç）ããããŸãã、åºæ¬çãªèãæ¹ã¯åé¡ãããŸãã。
Can a human adult stem cell spontaneously transform?
Correspondence re: Rubio, D., et al., Spontaneous human adult cell transformation. Cancer Res., 65: 3035-3039, 2005.
In vitro "Human adult stem cell transformation" is a major concern for those working on regenerative medicine or cell-based therapy. An article by Rubio et al. provides a caution that human mesenchymal stem cells undergo spontaneous transformation following long-term in vitro culture, i.e., 4 to 5 months. We agree that this was the first report of in vitro spontaneous transformation of human adult stem cells. Theoretically, normal human cells including mesenchymal stem cells have been shown to undergo a limited number of divisions in culture and then enter a non-dividing state referred to as "senescence" and do not spontaneously transform during culture period.
We have performed a similar experiment to determine if such chromosomal abnormality is detected after long-term in vitro culture of human mesenchymal stem cells or mesenchymal cells derived from bone marrow, umbilical cord, planceta, endometrium, and menstrual blood. Karyotypic analysis (G-banding and SKY) revealed that no genomic abnormalities except were found in the mesenchymal cells employed in this study. These abnormalities included translocations, a deletion, other rearrangements, and polyploidy. Our study raised some different points concerning chromosomal abnormality after long-term culture except for clonally inherited minor abnormalities. In addition, no telomerase activity was detected by the TRAP assay in the mesenchymal cells at all of the PDs tested, unlike in the case of multipotent adult progenitor cells (Verfaillie, et al.). Likewise, the telomere length of the mesenchymal cells decreased with the number of PDs.
We also monitored for in vivo malignant transformation of the mesenchymal cells for 3 months after inoculation and then sacrificed by cervical location. The cells did not undergo malignant transformation. They stopped dividing after reaching confluence, and they did not form any foci after confluence in vitro. Nor did the cells grafted into the subcutaneous and muscle tissue of nude mice or immunodeficient NOD/SCID/IL-2 receptor gamma-/- mice produce tumors, at least during the monitoring period (more than 100 days). Immunohistochemical analysis using an antibody against human specific vimentin revealed that injected mesenchymal cells survived but did not proliferate at the injection sites.
In the light that biosafety of mesenchymal stem cells as a source of cell-based therapy is very important, we, off course, should keep in mind that even a unlikely possiblity of human cell transformation during ex vivo expansion cannot be neglected and the human cell transformation may depend on culture condition employed in each laboratory or cell processing center. However, it should not escaped from our idea, i.e. almost zero expectation of spontaneous transformation of human adult stem cells after long-term ex vivo cultivation, obtained from our own results using cells derived from bone marrow, umbilical cord, planceta, endometrium, and menstrual blood.
We would not say the zero risk of spontaneous transformation during cultivation of mesenchymal stem cells and even one litterature (ref. 1) often win the title in this type of discussion to the controversy. However, we here emphasize that possiblity of spontaneous transformation in cultured human mesenchymal stem cell without treatment of storng mutagen or transfection of oncogenes is extremely low or considered to be nearly zero from the scientific viewpoint and tons of literature.
Sunday, August 12, 2007
倪éœã®å¡
o Novel markers for mesenchymal stem cell identification to enhance isolation and purification and to facilitate ex vivo stem cell expansion systems.
åŠäŒã§éè系幹现èããŒã«ã®è©±ãèãã。
CD106 (VCAM1)ãããã§ãããšããåçç ã®è©±。ãã®ããŒã«ãæãã现èã¯å¢æ®ããããšã®ããš。
å¥ã®ã°ã«ãŒããããã§CD133、CD271(NGFR, trk, p75, low-affinity nerve growth factor receptor)ããããšã®ããš。
ãã®åãã°ã«ãŒããããŠã¹ã§ã¯、CD140a (PDGFRalpha), Sca-1ããããšãããã話。
éè系幹现èããŒã«ã®è©±ã¯、ä»ã®å¹¹çŽ°èã«æ¯ã¹、æããã«é
ããŠãã。ãã®çç±ã¯、in vitro, in vivoã®ã¢ãã»ã€ãæšæºå（åãŠãå）ãããŠããªãããã§ãã。ããã¯å
ãè§、ãã£ãããšããç 究ã°ã«ãŒããããã®ãããªçºè¡šãããããšã¯æ¥µããŠå¥œãŸãã。æ¯é、確èªããŠã¿ãã。
倪éœã®å¡
Friday, August 10, 2007
Research question
Research areas of interest:
o Basic mesenchymal stem cell biology.
o Studies defining the lineage relationship between mesenchymal stem cells
and other stem cells.
o Novel markers for mesenchymal stem cell identification to enhance isolation
and purification and to facilitate ex vivo stem cell expansion systems.
o Refinement of cellular culture systems and elucidation of the molecular
events that permit ex vivo expansion of mesenchymal stem cells.
o Identification and characterization of functional, molecular regulators of
mesenchymal stem cell self-renewal and commitment.
o In vivo and in vitro assay systems for human mesenchymal stem cells.
o Role of growth factors, cytokines, receptors, transmembrane signaling,
marrow microenvironment, and adhesive proteins in mesenchymal stem cell
interactions and hematopoiesis.
o Identification and characterization of mechanisms by which mesenchymal stem
cells increase stem cell engraftment.
o Histocompatibility and allo-interactions, mechanism of induction of
transplant tolerance, minimizing the graft vs. host effect and graft
rejection for organ and cellular transplants of heart, lung, or blood
tissues.
o Studies on the biology of mesenchymal stem cells in aging including changes
in potential, population dynamics, mobilization, and interaction with the
aging environment.
o Basic research studies to develop future mesenchymal stem cell therapies to
correct genetic diseases or for repair or regeneration of tissue or organ
damage.
o Basic research studies to develop future gene therapy approaches using
mesenchymal stem cells as targets for gene insertion and long-term expression
of normal genes using viral and non-viral approaches to gene transduction.
Monday, July 16, 2007
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Friday, July 13, 2007
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Monday, July 9, 2007
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Monday, July 2, 2007
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Tuesday, June 26, 2007
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Thursday, June 21, 2007
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Tuesday, June 12, 2007
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Tuesday, June 5, 2007
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Tuesday, May 29, 2007
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æçµè¡ã«å«ãŸãã现èãå€ååèœãæããŠããå蚌ãšããŠ、åå®®äœéšã«ç±æ¥ããç¹åŸŽçãªè
«çã§ããçèè
«／æªæ§ãã¥ãŒã©ãŒç®¡æ··åè
«ç／äžèèæ§æ··åè
«çããã。ãããã¯ããããã²ãšã€ã®è
«çã«ã€ããããå称ã§ãã。åå®®äœéšã¯ãã¥ãŒã©ãŒç®¡ã«èµ·æºããã€ã®ã§、å€åœ©ãªçµç¹æèŠãå€ååèœãšçµã³ã€ãã解éã«ãã、ãã¥ãŒã©ãŒç®¡æ··åè
«çãšãåŒã°ãã。ãããã®è
«çã«ã¯、æå¹³äžç®æå、èè
«æåãå«ãŸã、暪çŽç、骚、è»éªšãšãã£ãçš®ã
ã®çŽ°èãèªãããã。ãã®è
«çã®ååšã、æçµè¡ç±æ¥çŽ°èãäžèè幹现èãšããŠã®æ¯ãèããããããšã瀺åããŠããæ§ãªæ°ãããŠãã。
Wednesday, May 23, 2007
æçµè¡ãšéªšæ Œçã®èå
æçµè¡ãšéªšæ Œçã®èåããããšã§、æ£åžžãã£ã¹ãããã£ã³ãä»äžãã。çãžã¹ãžã®æ²»çã«æå¹ãšèããŠãããŸã。
Friday, May 18, 2007
è»éªšçŽ°èã®åè£å 霢éçšã«ãããã±ã©ãã³äº€æ¿çŸè±¡
ããè»éªšçŽ°èãå¹é€ããŠãããš、ã±ã©ãã³ã®çš®é¡ãå€ãããã 。ã©ã£ã¡ãäžç®ã®äžéåŸç·ç¶ãšããŠç¥ãããŠãããã®ã§ãããã©ã。
é·ãçªèµ·ã䌞ã°ããéè系现èã¯、Tuj1éœæ§ãšãªã。
éè系现èã、çªèµ·äŒžåŒµãããšç¥çµããŒã«ãéœæ§ãšãªã。éã«、çªèµ·ã䌞匵ããŠããªã现èã¯、Tuj1é°æ§ã§ãã。ãã®ããšã¯、圢æ ãšããŒã«ãŒãçžé¢ããŠããããšãã、éè系现èãç¥çµçŽ°èãžã®ååããããšã匷ã瀺åããŠãã。
Saturday, May 5, 2007
èç€ã«ç±æ¥ããéè系现è
èç€ããç±æ¥ããéè系现èã¯、ãã®éšäœã«ãã£ãŠ、éãããã。Villous chorionã«ç±æ¥ããéè系现èã¯、ãããªã«å¢æ®ããªãããã。
http://www.ncbi.nlm.nih.gov/sites/entrez?tmpl=NoSidebarfile&db=PubMed&cmd=Retrieve&list_uids=17544394&dopt=Abstract
å€å°、æ·»ä»ããŠããå³ãšéããã©、è±æã®æ¹ãæ¬åœã§ã。ããããã。
Monday, April 30, 2007
äžæ»åãã现èã®çããé
æ、ããã£ãŒã®æã«、「ãããç§ã®çããé」ãšããã®ããã£ã。äžæ»åãã现èã®çããéã®äžã€ã«、å®å šæ§è©Šéšãšè¬å€ã®ã¹ã¯ãªãŒãã³ã°ãããããã。
现è寿åœ---骚é«é質现èã®å Žå
现è寿åœã¯、æ¡åããæ¹ã®å¹Žéœ¢ã«ãããã、æ¡åããçµç¹ã«ãäŸåãã。现èçš®ã«äŸåããã®ã¯、现è寿åœãã¹ãã¬ã¹ã«ããèŠå®ãã、ãã®ã¹ãã¬ã¹ã®æãæ¹ã现èããšã«éãã®ã§、åœç¶ãªæãããã。
Friday, April 27, 2007
Sunday, April 22, 2007
è¡æ¶²å¹¹çŽ°èãšé質现èã®é¢ä¿
4éãã®è¡æ¶²å¹¹çŽ°èãšé質现èã®é¢ä¿ããããŸã。äžçª、泚ç®ãããŠããã®ã¯、æã¯ãµã€ãã«ã€ã³ã§、ä»ã¯èäžã®ååã§ã。
Wednesday, April 18, 2007
Monday, April 16, 2007
Tuesday, April 10, 2007
现è移æ€：ãããŒçŽ°èãšãã¹ãçãšã®èå
ãããŒçŽ°èã¯、GFPã©ãã«。å ç«çµç¹ååŠã§æ€åº。
Monday, April 9, 2007
ãã幹现èãèªèããæäœ
Sunday, April 8, 2007
KUSA-A1现èãããã«éªšã。
KUSA-A1现èããŸã ãã£ãŠãã®ã。ãšãå±ããåããããšããã。ã§ã、KUSA-A1现èã£ãŠ、ãã®æåãªMC3T3-E1现èãã、ãã£ãšéªšèœçŽ°èãªãã ãã。
Saturday, April 7, 2007
åçå»çã®å¯Ÿè±¡çŸæ£
现è移æ€ãèããäžã§ã®å¯Ÿè±¡çŸæ£ã«å 倩æ§ä»£è¬çŸæ£ããããŸã。é µçŽ ãç£çãã现èãå©çšããããšã«ãã、é µçŽ è£å ãã§ãã。ããES现èã¯、beta-glucuronidaseãç£çããŸã。
Friday, April 6, 2007
ã»ã倪é
è§ç°å¹žå€«å
çãåœåãã「ã»ã倪é」。ã§ã。 å è€å®¹åå
çããã€ããã«ãªããŸãã。骚é«é質现èã®æ žãã、äœæããã¯ããŒã³çã§ã。倧奜ããªåçã§ã。
Biol Reprod. 70(2):415, 2004.
ã²ãã ã®è»¢åå¶éã、åé§çŽ°èãæç现èãã€ããã ã
çºçãé²ããšçŽ°èã¯å€ååèœã倱ã£ãŠãã，ããéããã现èã«ããååã§ããªããªã．å€ååèœãæãã现èãããã系統ã«ããååã§ããªã现èãžã®ç§»è¡ã¯，现èã®æœåšæ§ã®æ¶å€±ãŸãã¯éºäŒåçºçŸã®å¶éã«ã»ããªããªã．çµç¹ç¹ç°çãªéºäŒåã®çºçŸã¯，çµç¹ç¹ç°çãªè»¢åå åã«ãã転å掻æ§ãšçµç¹ç¹ç°çãªã²ãã ã®ã¡ãã«åã«ãã転åæå¶ããã，ã©ã¡ãã®åœ±é¿ããã匷ããã¯éºäŒåããšã«ç°ãªã．çµç¹å¹¹çŽ°èã®ååã«ãããå¶éã¯ã²ãã ã®ã¡ãã«åã«ãã、ãã®æ§é ãæèãæ¹å€ããããšãåçå»çããã现è転æã®ãã£ãããšãªã．
Monday, March 26, 2007
å¹é€çŽ°èã®å€åã®ãã«ãã
å¹é€ããŠãã现èã®ååã«é¢ããããã³ã·ã£ã«ã¯、å€ãããªã。è¡æ¶²çŽ°èã¯å¹é€ãç¶ããŠãè¡æ¶²çŽ°èã§ãã。ååç¶æ ã®å®å®æ§ãšå€åãããããšãã、ãããããã©ããã·ã«ã«ãªäºè±¡ãååãšããçŸè±¡ã®åºæ¬ã§ãã、転åå åã®ãããã¯ãŒã¯ã§ãã、ã²ãã ã®ã¡ãã«åã§ãã、ã²ãã ã®ã¡ãã«åããã®å®åžžç¶æ ãç£ã¿åºã．éã«å®åžžç¶æ ã、転åå åã®ãããã¯ãŒã¯、ã¡ãã«å、ã²ãã ã®ã¡ãã«åãåºå®ããŠããŸãããšãèããã、ãã®ç¶æ ã芳å¯ããã°ååã®å®åžžç¶æ ãã©ã®ã¬ãã«ã«ããããææã§ããããšã«ãªã．
Sunday, March 25, 2007
圢æ åŠçãªéªšé«é質现è
骚é«é質现èã®åœ¢æ
åŠçãªåé¡ã£ãŠ、ä»ã®æ代ã«ãªã£ãŠã倧äºã ã。ãã¡ãã、åå圢質ã§åé¡ããã®ãã¹ãžãšããã®ãåãããã©、åå圢質ã£ãŠã¹ãããªãããªããã。åèã¯èµ€ã§、éèã¯éã§æžãããŠããŸã。å®éã«ãã®ã¹ããŒã ããæãã«ãªã£ãã®ã¯、å®®å
最ææã ãšç解ããŠãããŸã。埮åŠã«ç¥çµãæãããŠããã®ãå³åã§ã。
PAA: Periarterial adventitial cells.
ISR: Intersinusoidal reticular cells.
PSA: Perisinusoidal adventitial cells.
è垯è¡ç±æ¥ã®éè系幹现è
è垯è¡ããéè现èãåé¢ã§ãããšããçºè¡šã次ã
ãšãªãããŠãã．åŸãããéè现èã¯èå
ç±æ¥ã§ãã、極ããŠå¢æ®èœåãé«ã．ãŸã、骚é«ç±æ¥ã®éè现èã«æ¯èŒããŠã寿åœãé·ããšæãã、åè£åæ°ãå€ã．è垯è¡ãã³ã¯ã«äœ¿ãããšãã§ããªãè¡æ¶²ãä»åŸã¯ç 究çšã«äœ¿çšããããšãå¯èœã«ãªãæç¶ããé²ããããŠãã、è垯è¡ã¯éè现èã®éèŠãªäŸçµŠæºã®ã²ãšã€ãšãªããã．éè系现èãšã¯éªš、è»éªš、èèª、éªšæ Œç、çç®、é垯、è
±ãšãã£ãçµåç¹çŽ°èãç·ç§°ããŠãã、çºçåŠçã«äžè»žäžèèç±æ¥ã®çŽ°èã§ãã。ãŸã、ãã®äžè»žäžèèã®ä»ã«、å¿ç、å¹³æ»ç、è¡ç®¡å
ç®ãšãã£ãçºçåŠçã«èåŽäžèèç±æ¥ã®çŽ°èããã．
è垯èªäœã¯、èå
ãšèç€ãã€ãªãã²ãã§ãã、è¡šé¢ã¯çŸèã®åå±€ç«æ¹äžç®ã§è¢«ãããŠãã．è垯ã¯、ïŒæ¬ã®èåè、ïŒæ¬ã®èéèãå«ã．ãããã®è¡ç®¡ã®éãåããŠããçµåçµç¹ã¯åå§çãªçµåçµç¹ã§ãã、è æ§çµç¹ãŸãã¯Wharton's jellyãšåŒã°ãã．è²èãªçªèµ·ãã®ã°ã现網现è（ããã§ã¯é質现èãŸãã¯éè系现èãšå矩）ãç²ã網ç®ããªã、现èé質ã«ã¯è åç·ç¶ãäžèŠåã«èµ°ã、åºè³ªã¯ã°ã«ã³ãµããã°ãªã«ã³（é
žæ§ã ã³å€ç³é¡）ã«å¯ãç²æ¶²æ§ã®ç©è³ªã§ã§ããŠãã．
ãã®ãããªè垯ã ãã«ååšããã®ã§ã¯ãªã、ããã«äŒŒãçµç¹ã¯èå
ã®çµåçµç¹ã«ãèŠããã．è霢ïŒã¶æãŸã§ã®çç®ã¯å¯å€©ã®ããã§ãã、ãã®ãããªçç®ã¯è æ§çµç¹ã®ç¶æ
ã«ãã．è垯è¡ã®éè系现èã®ç« ã§è垯ã®æ§é ãè°è«ããã®ã、è垯è¡ã®æ€äœã«å«ãŸããéè现èãè垯è¡ããšããšãã«è垯äžã«ãµããŸããWharton jellyã«ååšããéè现èãæ¡åãããŠããŸã£ãŠããå¯èœæ§ã¯åŠå®ã§ãã、æ¬åœã«è¡æ¶²äžã«å«ãŸããŠããã®ãã©ããã¯çåãæ®ã£ãŠããããã§ãã．Wharton jellyç±æ¥ã§ãããšããè°è«ã¯æ®ããã»ãšãã©ã®è«æã§ã¯è垯è¡ããããå²åã§éè系现èãæ¡åããããšããã®ãçŸåšã®ãšããã®çµè«ã§ãã．
ãã®è垯è¡ã®è°è«ã¯、æ«æ¢¢è¡ã§ãèšãããããããªã。
äžè»žäžèèãšèåŽäžèèã«ç±æ¥ããéè系现è
éè系现èãšã¯éªš、è»éªš、èèª、éªšæ Œç、çç®、é垯、è ±ãšãã£ãçµåç¹çŽ°èãç·ç§°ããŠãã、çºçåŠçã«äžè»žäžèèç±æ¥ã®çŽ°èã§ãã。ãŸã、ãã®äžè»žäžèèã®ä»ã«、å¿ç、å¹³æ»ç、è¡ç®¡å ç®ãšãã£ãçºçåŠçã«èåŽäžèèç±æ¥ã®çŽ°èããã．
Wednesday, March 21, 2007
éè系幹现è
ããŸããŸãªçµç¹ã«ç±æ¥ãã幹现èãè°è«ãããŠãã、「å¹é€ãã幹现èã¯、é è¡å¹¹çŽ°èã®ãããªå¹é€ããªã幹现èã«ããããã¢ãã»ã€ç³»ã¯åãæå³ãããŠãã？」、「éèç³»“å¹¹”现èãšãã£ãŠãããã©、å¹é€ããéçšã§“幹现è槔ãç²åŸããã®ã¯ãªãã ããã？」、「çäœå
ã§ã¯、éè系幹现èã¯æ¬åœã«å¹¹çŽ°èãšèšããã®ãã©ãã？」ããã®è«ç¹ã§ãã．éè系幹现èã®å€ååèœæ§ã¯Fibroblast colony-forming unitãšããã³ãããŒã«ç±æ¥ãã现èãå©çšããããã«、è©Šéšç®¡å
ã§ã®ã¢ãã»ã€ãšãªã。ãŸãã¯、ã²ãšã€ã®çŽ°èã«ç±æ¥ããã³ãããŒã§å€ååèœãæ€èšããæ¹æ³ãšåæã«、ã²ãšã€ã®çŽ°èãèå
èçœè³ªã§ã©ãã«ããŠå€ååèœãæ€èšããæ¹æ³ããã．幹现èã®å®çŸ©ã¯「èªå·±è€è£œãšå€ååèœæ§ãæãã现è」ã§ããããšããå¹é€ãå¢æ®ããæç¹ã§çŽ°èã¯èªå·±è€è£œèœãæããŠããèš³ã§ãã、å€ååèœãç²åŸããã°éèç³»ã«ç±æ¥ãã幹现èãšããããšã«ãªã£ãŠããŸã．å€ååèœæ§ã¯、è©Šéšç®¡å
ã§èªå°å€ãçšããã®ã§æ¥µç«¯ãªå Žåããªãã®çŽ°èã幹现èãšå€æãã、ååèœãæããŠããªãåãªãéè系现èã¯ç·ç¶èœçŽ°èãšåŒã°ããããšã«ãªã．é è¡å¹¹çŽ°èã¯å¹é€ãå¢æ®ãããããšã¯ããããããã®ã®CD34, CD133ãšãã£ãè¡šé¢ããŒã«ãŒãå©çšããŠåé¢ããããšãå¯èœã§ãã、幹现èãåå®ããã¢ãã»ã€ç³»ãå€ã．ãã®äžæ¹、å¹é€ãã幹现èã®ä»£è¡šãšããŠããããããã®ãšããŠ、èæ§å¹¹çŽ°èãšéè系幹现èãããããã．骚é«ã«ç±æ¥ããããéè系幹现èã®åé¢ã¯、「骚é«çŽ°èã«å¯ŸããŠ、CD29, 44, 73, 105, 166ãéœæ§æäœãšããŠ、CD14, 34, 45ãé°æ§æäœãšããŠäœ¿çšããããšã«ããéè系幹现èåç»ã®èªè」ããã．ãã®å Žåã¯、éè现èãäžåºŠãå¹é€ããããšãªã、骚é«ç©¿åºã«ãã£ãŠåŸããã骚é«çŽ°èããçŽæ¥、éè现èãåé¢ãã．è垯è¡ã«ç±æ¥ããéè系现èã¯æ°ã極端ã«å°ãªãããšãã、ãœãŒãããããšã¯æå³ããªããšèãããã．æ€äœå
šãŠãå¹é€ããŠãïŒåãªãããã以äžã§ãã．
é è¡ç³»å¹¹çŽ°è、èæ§å¹¹çŽ°è、éè系幹现èãšã§ã¯ç§åŠçãªæå³ã§å®çŸ©、ã¢ãã»ã€ç³»ãå«ããŠåã幹现èãšã¯èšããªã．å»çã«çšãããã骚é«é質现èã¯、å¹é€ç¿ã«ä»çã、å¢æ®ãããã®ãæãããšãå€ãããã©ã、å€ååèœãæããé質现èã«å
±éããææšãæ確ã«ããããšã¯èšåºçã«æ¥µããŠéèŠãªæ矩ãæã€．ããã«、ãããã®ææšã¯çºççç©åŠçã«åŠ¥åœã§ãã、ç¥çµå¹¹çŽ°è、äžç®çŽ°è、è¡æ¶²çŽ°èãšãã£ãä»ã®ç³»çµ±ã®çŽ°èãšã®å·®å¥åãå¯èœã§ããããšãå¿
èŠãšããããšåæã«æåç·ã®å»ççŸå Žã§æ€èšŒå¯èœãªçŸå®çãªãã®ã§ãªããŠã¯ãªããªã．ããã¯é è¡å¹¹çŽ°èãšéè系幹现èã®éãã ãã«ãããããšã§ã¯ãªã、ç¥çµå¹¹çŽ°è、èæ§å¹¹çŽ°è、Trophoblastic stem cells, è
žç®¡äžç®å¹¹çŽ°è、è幹现è、æ¯æ ¹å¹¹çŽ°è、çæ®å¹¹çŽ°è（EG cells)ãšãã£ãä»ã®å¹¹çŽ°èã«ãé¢ããåé¡ã§ãã．ãããã®éã§äœ¿çšãããŠãã「幹现è」ãšããåèªã®å®çŸ©ãç°ãªãããšãç§åŠè
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ãæããã«ãªããŸã§ã®é、èšèã®æ··ä¹±ãæŠå¿µã®æ··ä¹±ãããçšåºŠã¯é¿ããããªã．NIH/NIAã®æŽªå®æ°ã«ãã®ããšã京éœã®åŠäŒãçµãã£ãåŸã«å°ãããšãã、「ééã£ãŠãããã§ãã．」ãšäºåºŠã»ã©è¿äºãè²°ã£ã．
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骚é«é質现èã、ããã¡ã¢é·ã§èŠå®ãããReplicative senescence(M2)ãŸã§å¹é€å¯èœãšããå
·äœçãªæ¹æ³ã¯äœã？ 骚é«é質现èã®å¢æ®å¹å°ã«ã¯éåžž、è¡æž
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¥ããã ãã§ååã§ããããšã¯、骚é«ç±æ¥ã®éè系现èãšã¯ç°ãªã．骚é«ç±æ¥ã®éè系现èã¯、éåžžã®å¹å°ã§ã¯premature senescenceã«é¥ããã、p16/RBçµè·¯ãé»å®³ããå¿
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Sunday, February 4, 2007
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Friday, February 2, 2007
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Wednesday, January 31, 2007
Human ES cells with cardiomyogenic potential are positive for Flk-1 and CXCR2
Human ES cells with cardiomyogenic potential are positive for Flk-1 and CXCR2. Human ES cells are difficult to handle, i.e., low growth rate and low transfection efficiency.
Monday, January 29, 2007
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Friday, January 26, 2007
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Thursday, January 25, 2007
Galectin-1
Galectin-1 binds to integrin beta1 in neural stem cells. MSCs will be treated with galectin-1 to see if lectins can stimulate differentiation or growth of MSCs. The candidate for galectin-1 receptor in MSCs remains unclarified.
Tuesday, January 23, 2007
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