Evidence map›Paper›PMID 25445161›Full record

ArticleDigestive diseases and sciences2015

Bone Marrow Stromal Cells Inhibit the Activation of Liver Cirrhotic Fat-Storing Cells via Adrenomedullin Secretion.

Xiaodong Wang, Wei Zhao, Jinghua Wang, Kexin Shi, Xufu Qin, Qingfei Kong, Guangyou Wang, Lili Mu, Hulun Li, Bo Sun and 1 more

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Article in Digestive diseases and sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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11 authors.

Xiaodong WangEmergency Department, The 2nd Affiliated Hospital of Harbin Medical University, 148 Bao Jian Road, Nangang District, Harbin, 150086, China.
Wei Zhao
Jinghua Wang
Kexin Shi
Xufu Qin
Qingfei Kong
Guangyou Wang
Lili Mu
Hulun Li
Bo Sun
Lijun Shi

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCirrhosis, or liver fibrosis, which is mainly triggered by cirrhosis fat-storing cells (CFSCs) activation, has traditionally been considered an irreversible disease. However, recent observations indicate that even advanced fibrosis is still reversible by removing the causative agents. Anti-fibrotic effects of bone marrow-derived stromal cells (BMSCs) have been demonstrated by inhibiting CFSCs via cytokines secretion; however, the mechanisms are still unclear.

aimsThe purpose of this study was to explore the underlying mechanisms by which BMSCs modulate the function of activated CFSCs.

methodsAfter the co-culture of CFSCs with BMSCs supernatants with or without the addition of recombinant rat adrenomedullin (AM)/AM-specific siRNA, western blot analysis was mainly used to detect the differences of relative protein expression on CFSCs.

resultsBMSC-secreted adrenomedullin (AM) effectively inhibited the proliferation and activation of CFSCs by suppressing the expression of Ang II and its binding receptor, AT1, which resulted in a reduction of p47-phox formation.

conclusionsOur data suggested that BMSCs inhibited CFSC activation in vitro via the AM-Ang II-p47-phox signaling pathway, and since CFSC activation is an essential part of hepatic fibrosis process, this inhibition by BMSCs implies us new insights into the potential treatment of hepatic fibrosis via BMSCs.

Indexed as

Lipid MetabolismParacrine CommunicationActinsAdrenomedullinAngiotensin IIAnimalsCell ProliferationCells, CulturedCoculture TechniquesCollagen Type IHepatic Stellate CellsLiverLiver CirrhosisMesenchymal Stem CellsNADPH OxidasesRats, Sprague-DawleyActa2 protein, ratActinsAdrenomedullinAngiotensin IICollagen Type INADPH Oxidasesneutrophil cytosolic factor 1Receptor, Angiotensin, Type 1Receptor, Platelet-Derived Growth Factor betaTIMP1 protein, ratTissue Inhibitor of Metalloproteinase-1

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.