Vascular smooth muscle differentiation of murine stroma

Rémy-Martin, Jean Paul; Marandin, Aliette; Challier, Bruno; Bernard, G.; Deschaseaux, Marie; Hervé, P.; Wei, Yanzhang; Tsuji, Takashi; Auerbach, Robert; Dennis, James E.; Moore, Kateri; Greenberger, Joel S.; Charbord, Pierre

doi:10.1016/s0301-472x(99)00122-8

Cited by 48 publications

(44 citation statements)

References 65 publications

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“…The persistent expression of genes restricted to SMCs in PLA and ASC lead us to speculate that PLA cells might represent a hierarchical organization similar to that proposed to be operating in the bone marrow (35,36). Thus, the PLA population could be seen as a peripheral stromal cell compartment with cells displaying distinct differentiation capacities elicited by culture conditions or in vivo needs.…”

Section: Discussionmentioning

confidence: 84%

“…Some of these factors are known to be produced by endothelial cells, one of the cell types identified in PLA cultures. It has also been reported that the interaction of cell surface receptors and ligands, the formation of gap junction structures, as well as the involvement of short-rangeacting molecules between differentiated and stem cells contribute to stem cell differentiation (35). It is thus possible that cell-cell interaction among different cell types in the PLA may be important in smooth muscle differentiation of the progenitor cells.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Clonogenic multipotent stem cells in human adipose tissue differentiate into functional smooth muscle cells

Rodríguez¹,

Alfonso²,

Zhang³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

281

232

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Section: Discussionmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Clonogenic multipotent stem cells in human adipose tissue differentiate into functional smooth muscle cells

Rodríguez¹,

Alfonso²,

Zhang³

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

281

232

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“…33 Human LTBMC stromal cells are mesenchymal cells that follow a vascular smooth muscle cell differentiation pathway. 34,35 Detailed analysis of extracellular matrix and cytoskeletal protein expression in a variety of murine stromal cell lines led to the proposal of a model describing the sequential transition from immature mesenchymal to vascular smooth muscle-like stromal cells. 35 This model reflects the broad heterogeneity of the stroma and the need for cooperation among distinct stromal cell types for maintenance of hematopoiesis.…”

Section: Discussionmentioning

confidence: 99%

“…34,35 Detailed analysis of extracellular matrix and cytoskeletal protein expression in a variety of murine stromal cell lines led to the proposal of a model describing the sequential transition from immature mesenchymal to vascular smooth muscle-like stromal cells. 35 This model reflects the broad heterogeneity of the stroma and the need for cooperation among distinct stromal cell types for maintenance of hematopoiesis. Our analysis of membrane proteins in wild-type and IL-6 Ϫ/Ϫ stromal cultures showed increased expression in wild-type stroma of VCAM-1 and Sca-1, considered mesenchymal cell markers.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-6 deficiency affects bone marrow stromal precursors, resulting in defective hematopoietic support

Rodrı́guez

Bernad

Aracil

2004

Blood

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Interleukin-6 (IL-6) is a critical factor in the regulation of stromal function and hematopoiesis. In vivo bromodeoxyuridine incorporation analysis indicates that the percentage of Lin ؊ Sca-1 ؉ hematopoietic progenitors undergoing DNA synthesis is diminished in IL-6-deficient (IL-6 ؊/؊ ) bone marrow (BM) compared with wild-type BM. Reduced proliferation of IL-6 ؊/؊ BM progenitors is also observed in IL-6 ؊/؊ long-term BM cultures, which show defective hematopoietic support as measured by production of total cells, granulocyte macrophage-colony-forming units (CFU-GMs), and erythroid burstforming units (BFU-Es). Seeding experiments of wild-type and IL-6 ؊/؊ BM cells on irradiated wild-type or IL-6-deficient stroma indicate that the hematopoietic defect can be attributed to the stromal and not to the hematopoietic component. In IL-6 ؊/؊ BM, stromal mesenchymal precursors, fibroblast CFUs (CFU-Fs), and stroma-initiating cells (SICs) are reduced to almost 50% of the wild-type BM value. Moreover, IL-6 ؊/؊ stromata show increased CD34 and CD49e expression and reduced expression of the membrane antigens vascular cell adhesion molecule-1 (VCAM-1), Sca-1, CD49f, and Thy1. These data strongly suggest that IL-6 is an in vivo growth factor for mesenchymal precursors, which are in part implicated in the reduced longevity of the long-term repopulating stem cell compartment of IL-6 ؊/؊ mice. IntroductionInterleukin-6 (IL-6) is a multifunctional cytokine with a major role in inflammatory responses and is the primary inducer of acutephase proteins. 1 IL-6 also regulates the proliferation and differentiation of hematopoietic cells from several lineages at different maturation stages. 1 In synergy with IL-3, IL-6 stimulates proliferation of granulocyte-macrophage, megakaryocyte, and erythroid progenitors. [2][3][4][5] This cooperation has also been shown in several in vivo model systems designed to evaluate the effect of IL-6 on the stem cell compartment. 3,4,6 The specific contribution of IL-6 to homeostasis in the lymphohematopoietic system has been evaluated in the IL-6 Ϫ/Ϫ mouse model, which showed a clear reduction in the number of the earliest clonogenic precursors and in the function of long-term repopulating stem cells (LTRSCs). 7 IL-6 Ϫ/Ϫ mice show a decrease in absolute numbers of spleen colonyforming units (CFU-Ss) at day 12 and of pre-CFU-S hematopoietic progenitors, as well as a deficit in the LTRSC compartment. 7 In addition to the effects in early hematopoiesis, IL-6 Ϫ/Ϫ mice show defects in T-and B-cell function 8 and in acute-phase responses. 9 These results strongly suggest an important in vivo role for IL-6 in the survival and self-renewal of hematopoietic stem cells (HSCs) and early progenitors.IL-6 is produced by a variety of cells including T and B cells, macrophages, fibroblasts, bone marrow stromal cells, and mesenchymal cells. [10][11][12] The adherent stromal cell layer in long-term bone marrow cultures (LTBMCs) is necessary for balanced proliferation and differentiation of hematopoietic progenitors. 13 ...

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“…In contrast, there is recent compelling evidence that bone marrow-derived cells resident in the circulating blood invest in the neointima following vascular injury and can give rise to cells that express at least some properties of vascular SMCs (203,234). Alternatively, these circulating cells may fuse with resident SMCs and thus show colocalization of SMC markers and bone marrow lineage markers, although to date, no direct evidence for cell fusion in the vasculature has been shown.…”

Section: A Origin Of Intimal Smcs In Atherosclerotic Lesions: Media mentioning

confidence: 99%

Molecular Regulation of Vascular Smooth Muscle Cell Differentiation in Development and Disease

Owens

Kumar²,

Wamhoff³

2004

Physiological Reviews

2,987

3,134

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The focus of this review is to provide an overview of the current state of knowledge of molecular mechanisms/processes that control differentiation of vascular smooth muscle cells (SMC) during normal development and maturation of the vasculature, as well as how these mechanisms/processes are altered in vascular injury or disease. A major challenge in understanding differentiation of the vascular SMC is that this cell can exhibit a wide range of different phenotypes at different stages of development, and even in adult organisms the cell is not terminally differentiated. Indeed, the SMC is capable of major changes in its phenotype in response to changes in local environmental cues including growth factors/inhibitors, mechanical influences, cell-cell and cell-matrix interactions, and various inflammatory mediators. There has been much progress in recent years to identify mechanisms that control expression of the repertoire of genes that are specific or selective for the vascular SMC and required for its differentiated function. One of the most exciting recent discoveries was the identification of the serum response factor (SRF) coactivator gene myocardin that appears to be required for expression of many SMC differentiation marker genes, and for initial differentiation of SMC during development. However, it is critical to recognize that overall control of SMC differentiation/maturation, and regulation of its responses to changing environmental cues, is extremely complex and involves the cooperative interaction of many factors and signaling pathways that are just beginning to be understood. There is also relatively recent evidence that circulating stem cell populations can give rise to smooth muscle-like cells in association with vascular injury and atherosclerotic lesion development, although the exact role and properties of these cells remain to be clearly elucidated. The goal of this review is to summarize the current state of our knowledge in this area and to attempt to identify some of the key unresolved challenges and questions that require further study.

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Vascular smooth muscle differentiation of murine stroma

Cited by 48 publications

References 65 publications

Clonogenic multipotent stem cells in human adipose tissue differentiate into functional smooth muscle cells

Clonogenic multipotent stem cells in human adipose tissue differentiate into functional smooth muscle cells

Interleukin-6 deficiency affects bone marrow stromal precursors, resulting in defective hematopoietic support

Molecular Regulation of Vascular Smooth Muscle Cell Differentiation in Development and Disease

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