BMP4 inhibits myogenic differentiation of bone marrow–derived mesenchymal stromal cells in mdx mice

Cao, Ji; Li, Yaqin; Liang, Yingyin; Fei, Chen; Zhang, Huili; Zhu, Yunping; Yang, Juan; Shen, Feng; Zhang, Cheng

doi:10.1016/j.jcyt.2015.06.010

Cited by 10 publications

(5 citation statements)

References 21 publications

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“…Alcian blue staining was used to detect collagen production with chondrocyte differentiation 58 . Myocyte differentiation was induced by treating MSCs with 2% horse serum 59 . Cell nuclei were counterstained with 1 µg/ml of Hoechst 33258 (Sigma-Aldrich).…”

Section: Methodsmentioning

confidence: 99%

Adult stem cell deficits drive Slc29a3 disorders in mice

et al. 2019

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Mutations exclusively in equilibrative nucleoside transporter 3 (ENT3), the only intracellular nucleoside transporter within the solute carrier 29 ( SLC29 ) gene family, cause an expanding spectrum of human genetic disorders (e.g., H syndrome, PHID syndrome, and SHML/RDD syndrome). Here, we identify adult stem cell deficits that drive ENT3-related abnormalities in mice. ENT3 deficiency alters hematopoietic and mesenchymal stem cell fates; the former leads to stem cell exhaustion, and the latter leads to breaches of mesodermal tissue integrity. The molecular pathogenesis stems from the loss of lysosomal adenosine transport, which impedes autophagy-regulated stem cell differentiation programs via misregulation of the AMPK-mTOR-ULK axis. Furthermore, mass spectrometry-based metabolomics and bioenergetics studies identify defects in fatty acid utilization, and alterations in mitochondrial bioenergetics can additionally propel stem cell deficits. Genetic, pharmacologic and stem cell interventions ameliorate ENT3-disease pathologies and extend the lifespan of ENT3-deficient mice. These findings delineate a primary pathogenic basis for the development of ENT3 spectrum disorders and offer critical mechanistic insights into treating human ENT3-related disorders.

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Section: Methodsmentioning

confidence: 99%

Adult stem cell deficits drive Slc29a3 disorders in mice

et al. 2019

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“…Similarly, noggin treatment of bone marrow-derived mesenchymal stromal cells led to more dystrophin expression after engraftment into mice that lack dystrophin, a structural protein that maintains myofiber stability. On the contrary, Bmp4 treatment resulted in reduced dystrophin restoration [106]. Huang and colleagues found increased fat deposition in cardiotoxin-induced regenerating muscle of MyoD-Cre:Bmpr1a f/f and Myf5-Cre:Bmpr1a f/f mice.…”

Section: Regulation Of Adult Muscle Homeostasis and Regenerationmentioning

confidence: 99%

Bu-M-P-ing Iron: How BMP Signaling Regulates Muscle Growth and Regeneration

Borok

Mademtzoglou

Relaix

2020

JDB

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The bone morphogenetic protein (BMP) pathway is best known for its role in promoting bone formation, however it has been shown to play important roles in both development and regeneration of many different tissues. Recent work has shown that the BMP proteins have a number of functions in skeletal muscle, from embryonic to postnatal development. Furthermore, complementary studies have recently demonstrated that specific components of the pathway are required for efficient muscle regeneration.

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“…These cells do not fuse in the absence of myoblasts and rarely fuse with myoblasts in co-cultures [ 33 , 38 – 41 ]. However, bone marrow-derived MSCs could follow myogenic differentiation as the result of reprogramming induced by 5-azacytidine treatment, overexpression of Notch intracellular domain (NICD), paired box transcription factor 3 (Pax3), or constitutively active β-catenin, or as a result of 3D co-culture with myofibers [ 42 – 47 ]. It was also documented that bone marrow-derived MSCs could support skeletal muscle regeneration; however, these cells rarely participate in new myofiber formation [ 38 , 47 – 52 ].…”

Section: Introductionmentioning

confidence: 99%

Hypoxia preconditioned bone marrow-derived mesenchymal stromal/stem cells enhance myoblast fusion and skeletal muscle regeneration

et al. 2021

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Background The skeletal muscle reconstruction occurs thanks to unipotent stem cells, i.e., satellite cells. The satellite cells remain quiescent and localized between myofiber sarcolemma and basal lamina. They are activated in response to muscle injury, proliferate, differentiate into myoblasts, and recreate myofibers. The stem and progenitor cells support skeletal muscle regeneration, which could be disturbed by extensive damage, sarcopenia, cachexia, or genetic diseases like dystrophy. Many lines of evidence showed that the level of oxygen regulates the course of cell proliferation and differentiation. Methods In the present study, we analyzed hypoxia impact on human and pig bone marrow-derived mesenchymal stromal cell (MSC) and mouse myoblast proliferation, differentiation, and fusion. Moreover, the influence of the transplantation of human bone marrow-derived MSCs cultured under hypoxic conditions on skeletal muscle regeneration was studied. Results We showed that bone marrow-derived MSCs increased VEGF expression and improved myogenesis under hypoxic conditions in vitro. Transplantation of hypoxia preconditioned bone marrow-derived MSCs into injured muscles resulted in the improved cell engraftment and formation of new vessels. Conclusions We suggested that SDF-1 and VEGF secreted by hypoxia preconditioned bone marrow-derived MSCs played an essential role in cell engraftment and angiogenesis. Importantly, hypoxia preconditioned bone marrow-derived MSCs more efficiently engrafted injured muscles; however, they did not undergo myogenic differentiation.

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BMP4 inhibits myogenic differentiation of bone marrow–derived mesenchymal stromal cells in mdx mice

Cited by 10 publications

References 21 publications

Adult stem cell deficits drive Slc29a3 disorders in mice

Adult stem cell deficits drive Slc29a3 disorders in mice

Bu-M-P-ing Iron: How BMP Signaling Regulates Muscle Growth and Regeneration

Hypoxia preconditioned bone marrow-derived mesenchymal stromal/stem cells enhance myoblast fusion and skeletal muscle regeneration

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