Liver from bone marrow in humans

Theise, Neil D.; Nimmakayalu, Manjunath; Gardner, Rebekah; Illei, Peter B.; Morgan, G. W.; Teperman, Lewis; Henegariu, Octavian; Krause, Diane S.

doi:10.1053/jhep.2000.9124

Cited by 1,132 publications

(806 citation statements)

References 29 publications

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“…To permit exposure of type II collagen to the primary antibody, sections were digested with 0.1 U/mL of chondroitinase ABC in 1% (w/v) BSA in DPBS for 45 minutes and were then exposed to 1 mg/mL pronase (Calbiochem, LaJolla, CA, USA) for 30 minutes. Sections were incubated for 1 hour with the type II collagen-specific antibody (II-II6B3) diluted at 1:100 in 1% BSA in DPBS [20,43]. The IIII6B3 antibody was developed by T. Linsenmayer and was obtained from the Developmental Studies Hybridoma Bank maintained by the University of Iowa, Department of Biological Sciences, Iowa City, IA, USA.…”

Section: Immunofluorescencementioning

confidence: 99%

“…Adult-derived stem cells that can be harvested from bone, fat, or muscle offer alternative sources for chondrocytes [8][9][10][11]. These tissues have been demonstrated to contain stem cells of mesenchymal origin, which have potential to differentiate into various specific tissue cell phenotypes that include tendon, fat, marrow stroma, dermis, muscle, bone, and cartilage [10,[12][13][14][15][16][17][18][19][20]. Numerous studies have demonstrated that bone marrow-derived mesenchymal stem cells (MSCs) can give rise to chondrocytes under appropriate conditions [21][22][23].…”

Section: Introductionmentioning

confidence: 99%

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Adenoviral-mediated transfer of TGF-β1 but not IGF-1 induces chondrogenic differentiation of human mesenchymal stem cells in pellet cultures

Kawamura¹,

Chu²,

Sobajima³

et al. 2005

Experimental Hematology

102

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Objective. The objective of the present study was to investigate the potential of application of growth factor genes to induce chondrogenic differentiation of human-derived mesenchymal stem cells (MSCs). The growth factor genes evaluated in the present study were transforming growth factor 1 (TGF-β1) and insulin-like growth factor 1 (IGF-1).Methods. Human MSCs were transduced with the adenoviral vectors carrying either TGF-β1 or IGF-1 (AdTGF-β1 and AdIGF-1 respectively) or a combination of both growth factor genes at different multiplicities of infection (MOI) and were then made into pellets. Pellets were also made from nontransduced cells and maintained in culture medium supplemented with 10 ng/mL of TGF-β1. At specified time points, histological analysis, cartilage matrix gene expression, and immunofluorescence were performed to determine the extent of chondrogenic differentiation.Results. MSCs transduced with the AdTGF-β1 demonstrated robust chondrogenic differentiation, while those made from AdIGF-1 did not. AdTGF-β1 pellets demonstrated aggrecan gene expression as early as day 3 of pellet culture, while type II collagen gene expression was detected by day 10 of culture. The AdIGF-1, alone or in combination with TGF-β1 pellets, did not show any type II collagen gene expression at any time point. By immunofluoresecence, type X collagen was distributed throughout the matrix in TGF-β1 protein pellets while the growth factor gene pellets displayed scant staining. Conclusion.The results suggest that sustained administration of TGF-β1 may be more effective in suppressing terminal differentiation than intermittent dosing and thus effective for cartilage repair.

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Section: Immunofluorescencementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Adenoviral-mediated transfer of TGF-β1 but not IGF-1 induces chondrogenic differentiation of human mesenchymal stem cells in pellet cultures

Kawamura¹,

Chu²,

Sobajima³

et al. 2005

Experimental Hematology

102

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“…Consistent with this premise, hematopoietic stem cells (HSCs) have been shown to transdifferentiate into cells of the hepatocytic lineage in both rodents and humans [16][17][18][19][20][21][22][23]. However, these findings have been challenged by studies showing that cell fusion rather than transdifferentiation of HSCs is involved in regeneration [24,25] and that bone marrow (BM) does not contribute as source of expanding oval cells [26].…”

Section: Introductionmentioning

confidence: 99%

Characterization of two distinct liver progenitor cell subpopulations of hematopoietic and hepatic origins

Corcelle¹,

Stieger

Gjinovci³

et al. 2006

Experimental Cell Research

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Despite extensive studies, the hematopoietic versus hepatic origin of liver progenitor oval cells remains controversial. The aim of this study was to determine the origin of such cells after liver injury and to establish an oval cell line. Rat liver injury was induced by subcutaneous insertion of 2-AAF pellets for 7 days with subsequent injection of CCl 4 . Livers were removed 9 to 13 days post-CCl 4 treatment. Immunohistochemistry was performed using anti-c-kit, OV6, Thy1, CK19, AFP, vWF and Rab3b. Isolated non-parenchymal cells were grown on mouse embryonic fibroblast, and their gene expression profile was characterized by RT-PCR. We identified a subpopulation of OV6/CK19/Rab3b-expressing cells that was activated in the periportal region of traumatized livers. We also characterized a second subpopulation that expressed the HSCs marker c-kit but not Thy1. Although we successfully isolated both cell types, OV6/CK19/Rab3b + cells fail to propagate while c-kit + -HSCs appeared to proliferate for up to 7 weeks. Cells formed clusters which expressed c-kit, Thy1 and albumin. Our results indicate that a bona fide oval progenitor cell population resides within the liver and is distinct from c-kit + -HSCs. Oval cells require the hepatic niche to proliferate, while cells mobilized from the circulation proliferate and transdifferentiate into hepatocytes without evidence of cell fusion.

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“…4 Numerous studies conducted on animal models and human beings have suggested that bone marrow cells (BMCs) may give rise to OCs. [5][6][7][8][9] In vitro studies also have shown that a subpopulation of BMCs expresses hepatic markers and, conversely, that OCs express hematopoietic antigens such as CD34, c-kit, and Thy-1. 10,11 Mobilization of BMCs into the circulation can be induced by a wide variety of molecules such as cytoreductive drugs, chemokines, and hematopoietic cytokines.…”

mentioning

confidence: 99%

Granulocyte–Colony Stimulating Factor Promotes Liver Repair and Induces Oval Cell Migration and Proliferation in Rats

et al. 2007

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Background & Aims-Hepatic regeneration is a heterogeneous phenomenon involving several cell populations. Oval cells are considered liver stem cells, a portion of which derive from bone marrow (BM). Recent studies have shown that granulocyte-colony stimulating factor (G-CSF) may be effective in facilitating liver repair. However, it remains unclear if G-CSF acts by mobilizing BM cells, or if it acts locally within the liver microenvironment to facilitate the endogenous restoration program. In the present study, we assessed the involvement of G-CSF during oval cell activation.

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Liver from bone marrow in humans

Cited by 1,132 publications

References 29 publications

Adenoviral-mediated transfer of TGF-β1 but not IGF-1 induces chondrogenic differentiation of human mesenchymal stem cells in pellet cultures

Adenoviral-mediated transfer of TGF-β1 but not IGF-1 induces chondrogenic differentiation of human mesenchymal stem cells in pellet cultures

Characterization of two distinct liver progenitor cell subpopulations of hematopoietic and hepatic origins

Granulocyte–Colony Stimulating Factor Promotes Liver Repair and Induces Oval Cell Migration and Proliferation in Rats

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