Osteogenic differentiation of mesenchymal stem cells is impaired by bone morphogenetic protein 7

Wongwitwichot, Paweena; Kaewsrichan, Jasadee

doi:10.1016/j.advms.2016.12.001

Cited by 9 publications

(9 citation statements)

References 23 publications

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“…The various biological properties and distinct involved pathways in different cell lines might contribute to our contrary results. Considering sharing certain receptors with BMP7 in the signaling pathway (Suzuki et al, 1997) (Wongwitwichot & Kaewsrichan, 2017). Another study also showed the variability of BMP7 in the osteogenic regulation.…”

Section: Discussionmentioning

confidence: 96%

MiR‐137 knockdown promotes the osteogenic differentiation of human adipose‐derived stem cells via the LSD1/BMP2/SMAD4 signaling network

Fan

Wang

et al. 2019

Journal Cellular Physiology

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MicroRNAs are a group of endogenous regulators that participate in several cellular physiological processes. However, the role of miR-137 in the osteogenic differentiation of human adipose-derived stem cells (hASCs) has not been reported. This study verified a general downward trend in miR-137 expression during the osteogenic differentiation of hASCs. MiR-137 knockdown promoted the osteogenesis of hASCs in vitro and in vivo. Mechanistically, inhibition of miR-137 activated the bone morphogenetic protein 2 (BMP2)-mothers against the decapentaplegic homolog 4 (SMAD4) pathway, whereas repressed lysine-specific histone demethylase 1 (LSD1), which was confirmed as a negative regulator of osteogenesis in our previous studies. Furthermore, LSD1 knockdown enhanced the expression of BMP2 and SMAD4, suggesting the coordination of LSD1 in the osteogenic regulation of miR-137. This study indicated that miR-137 negatively regulated the osteogenic differentiation of hASCs via the LSD1/BMP2/SMAD4 signaling network, revealing a new potential therapeutic target of hASC-based bone tissue engineering.

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Section: Discussionmentioning

confidence: 96%

MiR‐137 knockdown promotes the osteogenic differentiation of human adipose‐derived stem cells via the LSD1/BMP2/SMAD4 signaling network

Fan

Wang

et al. 2019

Journal Cellular Physiology

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“…EGF and FGF are widely confirmed to promote ADSCs cell proliferation and epithelial differentiation [ 26 ]. However, as a member of the transforming growth factor β (TGF-β) superfamily, BMP7 negatively regulate RUNX2 expression [ 27 ]. So, we made these change to improve our induction system.…”

Section: Discussionmentioning

confidence: 99%

RUNX2 promotes epithelial differentiation of ADSCs and burn wound healing via targeting E-cadherin

Zhao

Xia

et al. 2017

Oncotarget

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Epithelial differentiation of adipose-derived stem cells (ADSCs) is mediated by sophisticated interactions of various molecular functions and biological processes, including transcriptional regulation. Runt-related transcription factor 2 (RUNX2) increases osteoblast and adipocyte differentiation of ADSCs. However, the role of RUNX2 in epithelial differentiation of ADSCs is unknown. We first showed that ADSCs possess the potential to differentiate into epithelial lineage. Then, we employed the effect of RUNX2 on epithelial differentiation of ADSCs. Our data showed that RUNX2 promoted epithelial differentiation of ADSCs. Overexpression or knockdown of RUNX2 resulted in increase or decrease of E-cadherin expression, respectively. Abatement of E-cadherin in ADSCs attenuated RUNX2-activated epithelial conversion of ADSCs and epithelial markers cytokeratin 18 (CK18) and zonula occludens protein-1 (ZO-1). We also evaluated the effect of RUNX2 on burn wound healing in vivo. The wound re-epithelialization were accelerated by RUNX2. The wound closure indexs, demis regeneration and revascularization were all improved. Furthermore, RUNX2 binding directly to the E-cadherin promoter region was characterized in ADSCs by chromatin immunoprecipitation (ChIP) and luciferase promoter reporter assays. Taken together, the study demonstrates the role of RUNX2 in epithelial differentiation of ADSCs and suggests that RUNX2 promotes E-cadherin expression, at least in part, through its direct binding to the promoter.

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“…BMP-2 and BMP-4 have also been most associated with calcific arteriopathy [177], although BMP7 might exert inhibitory effects against VC [176]. In bone formation, both BMP2 and BMP7 induce osteoblast differentiation, through increased expression of runt-related transcription factor 2 (Runx2) and osterix [178][179][180].…”

Section: Bone Morphogenic Protein (Bmp)2mentioning

confidence: 99%

Vascular Calcification—New Insights into Its Mechanism

Lee

Jeon

2020

IJMS

283

254

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Vascular calcification (VC), which is categorized by intimal and medial calcification, depending on the site(s) involved within the vessel, is closely related to cardiovascular disease. Specifically, medial calcification is prevalent in certain medical situations, including chronic kidney disease and diabetes. The past few decades have seen extensive research into VC, revealing that the mechanism of VC is not merely a consequence of a high-phosphorous and -calcium milieu, but also occurs via delicate and well-organized biologic processes, including an imbalance between osteochondrogenic signaling and anticalcific events. In addition to traditionally established osteogenic signaling, dysfunctional calcium homeostasis is prerequisite in the development of VC. Moreover, loss of defensive mechanisms, by microorganelle dysfunction, including hyper-fragmented mitochondria, mitochondrial oxidative stress, defective autophagy or mitophagy, and endoplasmic reticulum (ER) stress, may all contribute to VC. To facilitate the understanding of vascular calcification, across any number of bioscientific disciplines, we provide this review of a detailed updated molecular mechanism of VC. This encompasses a vascular smooth muscle phenotypic of osteogenic differentiation, and multiple signaling pathways of VC induction, including the roles of inflammation and cellular microorganelle genesis.

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Osteogenic differentiation of mesenchymal stem cells is impaired by bone morphogenetic protein 7

Cited by 9 publications

References 23 publications

MiR‐137 knockdown promotes the osteogenic differentiation of human adipose‐derived stem cells via the LSD1/BMP2/SMAD4 signaling network

MiR‐137 knockdown promotes the osteogenic differentiation of human adipose‐derived stem cells via the LSD1/BMP2/SMAD4 signaling network

RUNX2 promotes epithelial differentiation of ADSCs and burn wound healing via targeting E-cadherin

Vascular Calcification—New Insights into Its Mechanism

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