Human Stem/Progenitor Cells from Bone Marrow Enhance Glial Differentiation of Rat Neural Stem Cells: A Role for Transforming Growth Factor β and Notch Signaling

Robinson, Andrew P.; Foraker, Jessica; Ylöstalo, Joni; Prockop, Darwin J.

doi:10.1089/scd.2009.0444

Cited by 36 publications

(39 citation statements)

References 52 publications

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“…Moreover, PDGF, PGF and TGF β are known to increase survival and proliferation of oligodendrocytes63. BDNF also increases oligodendrocyte proliferation and BMP 1 signaling mediates astrocyte differentiation of oligodendrocyte progenitor cells64. SPARC has been shown to modulate several growth factor signaling cascades (i.e., VEGF (vascular endothelial growth factor), PDGF (platelet-derived growth factor), FGF2 (fibroblast growth factor-2), and TGF (transforming growth factor beta)) and can regulate integrin-mediated adhesion6566.…”

Section: Discussionmentioning

confidence: 99%

Modulation properties of factors released by bone marrow stromal cells on activated microglia: an in vitro study

Cizkova

Devaux

Marrec-Croq

et al. 2014

Sci Rep

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In the present paper we develop a new non-cell based (cell-free) therapeutic approach applied to BV2 microglial cells and spinal cord derived primary microglia (PM) using conditioned media from rat bone marrow stromal cells (BMSCs-CM). First we collected conditioned media (CM) from either naive or injured rat spinal cord tissue (SCI-CM, inflammatory stimulation agent) and from rat bone marrow stromal cells (BMSCs-CM, therapeutic immunomodulation agent). They were both subsequently checked for the presence of chemokines and growth, neurotrophic and neural migration factors using proteomics analysis. The data clearly showed that rat BMSCs-CM contain in vitro growth factors, neural migration factors, osteogenic factors, differentiating factors and immunomodulators, whereas SCI-CM contain chemokines, chemoattractant factors and neurotrophic factors. Afterwards we determined whether the BMSCs-CM affect chemotactic activity, NO production, morphological and pro-apoptotic changes of either BV2 or PM cells once activated with SCI-CM. Our results confirm the anti-migratory and NO-inhibitory effects of BMSCs-CM on SCI-CM-activated microglia with higher impact on primary microglia. The cytotoxic effect of BMSCs-CM occurred only on SCI-CM-stimulated BV2 cells and PM, not on naive BV2 cells, nor on PM. Taken together, the molecular cocktail found in BMSCs-CM is favorable for immunomodulatory properties.

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Section: Discussionmentioning

confidence: 99%

Modulation properties of factors released by bone marrow stromal cells on activated microglia: an in vitro study

Cizkova

Devaux

Marrec-Croq

et al. 2014

Sci Rep

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“…The ability of TGF-␤1 to mediate transdifferentiation of cells into another lineage has been well described with the use of numerous cell systems. [38][39][40][41] Indeed, TGF-␤ family members play important roles in epithelial-mesenchymal transformation during normal development and in pathologic conditions and can redirect differentiation along mesenchymal lineages (for adipocytes, osteoblasts, or chondrocytes) in response to TGF-␤ or bone morphogenetic protein signals. TGF-␤1, in particular, has been characterized as being able to regulate expression of endothelial markers; exogenous administration of TGF-␤1 increased endothelialspecific expression in mouse embryoid bodies and inhibited expression of endodermal markers.…”

Section: Discussionmentioning

confidence: 99%

TGF-β1 signaling and Krüppel-like factor 10 regulate bone marrow–derived proangiogenic cell differentiation, function, and neovascularization

Wara

Foo

Croce

et al. 2011

Blood

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Emerging evidence demonstrates that proangiogenic cells (PACs) originate from the BM and are capable of being recruited to sites of ischemic injury where they contribute to neovascularization. We previously determined that among hematopoietic progenitor stem cells, common myeloid progenitors (CMPs) and granulocyte-macrophage progenitor cells (GMPs) differentiate into PACs and possess robust angiogenic activity under ischemic conditions. Herein, we report that a TGF-␤1-responsive Krü ppellike factor, KLF10, is strongly expressed in PACs derived from CMPs and GMPs, ϳ 60-fold higher than in progenitors lacking PAC markers. KLF10 ؊/؊ mice present with marked defects in PAC differentiation, function, TGF-␤ responsiveness, and impaired blood flow recovery after hindlimb ischemia, an effect rescued by wild-type PACs, but not KLF10 ؊/؊ PACs. Overexpression studies revealed that KLF10 could rescue PAC formation from TGF-␤1 ؉/؊ CMPs and GMPs. Mechanistically, KLF10 targets the VEGFR2 promoter in PACs which may underlie the observed effects. These findings may be clinically relevant because KLF10 expression was also found to be significantly reduced in PACs from patients with peripheral artery disease. Collectively, these observations identify TGF-␤1 signaling and KLF10 as key regulators of functional PACs derived from CMPs and GMPs and may provide a therapeutic target during cardiovascular ischemic states. (Blood. 2011;118(24):6450-6460) IntroductionAccumulating evidence suggests that in healthy persons, circulating endothelial progenitor cells, broadly defined as proangiogenic cells (PACs), represent a population of BM-derived stem and progenitor cells responsible for repairing injured tissue and initiating neovasculogenesis. 1,2 Potentiation of PAC mobilization, homing, or adhesion has been shown to ameliorate the development of ischemic injury in animal models. 1,2 In addition, blockade of proangiogenic cytokines or their signaling pathways is believed to alter PAC function and to lead to impaired angiogenesis in response to vascular injury and in end-organ ischemia. 1,2 Indeed, reduced levels of circulating PACs and diminished PAC function have been reported and found to correlate with a wide spectrum of atherosclerotic vascular diseases, including peripheral artery disease (PAD). [3][4][5] Several early phase 1/2 trials have been conducted to assess the efficacy of cell-based therapies to treat patients with PAD but have yielded mixed results. 1,2,6-9 Identification of specific PAC subtypes that are endowed with superior capacity to promote neovascularization may represent a particularly efficacious therapeutic strategy. We have demonstrated that among hematopoietic progenitor stem cells, the common myeloid progenitors (CMPs) and granulocytemacrophage progenitors (GMPs) constitute a population of BMderived cells that preferentially differentiate into PACs and possess robust angiogenic activity under ischemic conditions in vivo. 10 However, the signaling pathways and downstream factors that mediate these proangiogenic...

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“…For instance, coculturing human MSCs (hMSCs) with rat neural stem cells (rNSCs) was found to stimulate astrocyte and oligodendrocyte differentiation of the rNSCs, driven by increased secretion of soluble factors such as TGF-β1 by the hMSCs and probably through the Notch pathway [66] . In addition, when using a mouse midbrain embryonic day (E) 12 neurospheres culture as an experimental model, TGF-β can cooperate with persephin for dopaminergic phenotype induction through receptor-mediated differentiation signaling, involving p38 kinase and PI3K/AKT pathways [67] .…”

Section: Tgf-β In Other Differentiationsmentioning

confidence: 99%

Different roles of TGF-β in the multi-lineage differentiation of stem cells

Wang¹

2012

WJSC

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Stem cells are a population of cells that has infinite or long-term self-renewal ability and can produce various kinds of descendent cells. Transforming growth factor β (TGF-β) family is a superfamily of growth factors, including TGF-β1, TGF-β2 and TGF-β3, bone morphogenetic proteins, activin/inhibin, and some other cytokines such as nodal, which plays very important roles in regulating a wide variety of biological processes, such as cell growth, differentiation, cell death. TGF-β, a pleiotropic cytokine, has been proved to be differentially involved in the regulation of multi-lineage differentiation of stem cells, through the Smad pathway, non-Smad pathways including mitogen-activated protein kinase pathways, phosphatidylinositol-3-kinase/AKT pathways and Rholike GTPase signaling pathways, and their cross-talks. For instance, it is generally known that TGF-β promotes the differentiation of stem cells into smooth muscle cells, immature cardiomyocytes, chondrocytes, neurocytes, hepatic stellate cells, Th17 cells, and dendritic cells. However, TGF-β inhibits the differentiation of stem cells into myotubes, adipocytes, endothelial cells, and natural killer cells. Additionally, TGF-β can provide competence for early stages of osteoblastic differentiation, but at late stages TGF-β acts as an inhibitor. The three mammalian isoforms (TGF-β1, 2 and 3) have distinct but overlapping effects on hematopoiesis. Understanding the mechanisms underlying the regulatory effect of TGF-β in the stem cell multi-lineage differentiation is of importance in stem cell biology, and will facilitate both basic research and clinical applications of stem cells. In this article, we discuss the current status and progress in our understanding of different mechanisms by which TGF-β controls multi-lineage differentiation of stem cells.

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Human Stem/Progenitor Cells from Bone Marrow Enhance Glial Differentiation of Rat Neural Stem Cells: A Role for Transforming Growth Factor β and Notch Signaling

Cited by 36 publications

References 52 publications

Modulation properties of factors released by bone marrow stromal cells on activated microglia: an in vitro study

Modulation properties of factors released by bone marrow stromal cells on activated microglia: an in vitro study

TGF-β1 signaling and Krüppel-like factor 10 regulate bone marrow–derived proangiogenic cell differentiation, function, and neovascularization

Different roles of TGF-β in the multi-lineage differentiation of stem cells

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