Potential Roles of BMP9 in Liver Fibrosis

Bi, Jianjun; Ge, Shengfang

doi:10.3390/ijms151120656

Cited by 42 publications

(30 citation statements)

References 73 publications

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“…BMP9 is specifically expressed in the liver tissue and may induce liver fibrosis through ALK1, endoglin, Id1, hepcidin and Snail [11]. BMP7 has been shown to inhibit TGFβ dependent epithelial to mesenchymal transition (EMT) of hepatocytes and also has an antiapoptotic and anti-inflammatory effect [10].…”

mentioning

confidence: 99%

Bone morphogenetic proteins in inflammation, glucose homeostasis and adipose tissue energy metabolism

Grgurević

Christensen

Schulz

et al. 2016

Cytokine & Growth Factor Reviews

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mentioning

confidence: 99%

Bone morphogenetic proteins in inflammation, glucose homeostasis and adipose tissue energy metabolism

Grgurević

Christensen

Schulz

et al. 2016

Cytokine & Growth Factor Reviews

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“…Thus, a few BMP members have been applied clinically to treat the bone related diseases, such as bone repair and spine fusion . BMP9, also named growth differentiation factor 2 (GDF2), was also reported to have a potency for facilitating osteogenic differentiation after it first was isolated in fetal mouse liver and expressed in hepatocytes with influences for liver diseases . BMPs exert their function through BMP/Smad signal mainly.…”

Section: Discussionmentioning

confidence: 99%

Inhibin α‐subunit inhibits BMP9‐induced osteogenic differentiation through blocking BMP/Smad signal and activating NF‐κB signal in mesenchymal stem cells

Huang

Cheng²,

Jitao³

et al. 2018

J of Cellular Biochemistry

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Inhibin-α, a member of the transforming growth factor (TGF-β) superfamily, has been involved in bone turnover during the menopausal transition via endocrine effects, and it was previously reported that inhibins may antagonize the function of BMPs. Certainly, one of the most important functions of BMPs is to induce osteogenic differentiation. BMP9 as one of the most potent BMPs to induce osteogenic differentiation has gotten more and more attentions. Nonetheless, the effects of inhibin-α on osteogenesis remain unknown. Besides, mesenchymal stem cells (MSCs) with the ability to differentiate into multiple mesenchymal lineages, including osteoblasts, adipocyte, chondrocytes, and myoblasts in vitro, have become the promising seed cells for bone tissue engineering. Here, we investigated the role of inhibin-α on BMP9-induced osteogenic differentiation in MSCs and tried to discover the mechanism underlying this process. We found inhibin-α apparently reduced the classical osteogenic markers and the ectopic bone formation induced by BMP9. In addition, the ratio of OPG to RANKL is declined also in the presence of inhibin-α. For mechanism, we found that exogenous expression of inhibin-α inhibits BMP9-induced osteogenic differentiation through blocking BMP/Smad signal transduction and activating NF-κB signal which is repressed by BMP9. Thus, our findings indicated that inhibin-α has a negative effect on BMP9-induced osteogenic differentiation in MSCs, which may provide a novel insight into the regulation of skeletal development and new strategy for bone tissue engineering.

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“…BMP2, BMP4, BMP 7, and BMP 9 are known to be involved in fibrosis of the liver. 23,24,25 BMP signal starts from BMP binding with its serine/ threonine kinase receptor ie BMP type I and type II receptor. BMPs that bind to BMPR II will cause type II receptors to phosphorylate serine and threonine residues at BMP type I receptor.…”

Section: Bmp Receptorsmentioning

confidence: 99%

Role of Serin/ Threonine Kinase Inhibitor in Therapy Non-Alcoholic Steatohepatitis and Alcoholic Hepatitis

Lestari¹

2019

JKK

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Liver fibrosis is a reversible response to a wound healing with marked accumulation of extracellular matrix which caused by injury to the liver. Liver fibrosis can be caused by various factors including alcohol and non-alcohol steatohepatitis. The process of fibrosis serves to localize the inflammation during chronic exposure. The hepatic stem cell (HSC) has a key role in the pathogenesis of liver fibrosis. The HSC activation is characterized by increased profibrogenic mediators including members of the TGF-? superfamily. In order to enable signal transduction, the mediator needs to bind to its receptors. The serine/ threonine kinase receptor is a receptor that binds to the TGF-? superfamily ligand, including TGF-?, BMP, activin and other mediators. The ligand receptor-binding activity will stimulate signal transduction that will translocate into the nucleus and phosphorylate various transcription factors that play a role in cell proliferation, differentiation, or apoptosis. There is currently no standard therapy for liver fibrosis. Based on the central role of the serine/ threonine kinase receptor in the pathogenesis of liver fibrosis, it is thought that the use of serine/ threonine kinase inhibitors is a promising therapy.

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Potential Roles of BMP9 in Liver Fibrosis

Cited by 42 publications

References 73 publications

Bone morphogenetic proteins in inflammation, glucose homeostasis and adipose tissue energy metabolism

Bone morphogenetic proteins in inflammation, glucose homeostasis and adipose tissue energy metabolism

Inhibin α‐subunit inhibits BMP9‐induced osteogenic differentiation through blocking BMP/Smad signal and activating NF‐κB signal in mesenchymal stem cells

Role of Serin/ Threonine Kinase Inhibitor in Therapy Non-Alcoholic Steatohepatitis and Alcoholic Hepatitis

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