Apelin attenuates the osteoblastic differentiation of vascular smooth muscle cells.

Vascular calcification, which results from a process osteoblastic differentiation of vascular smooth muscle cells (VSMCs), is a major risk factor for cardiovascular morbidity and mortality. Apelin is a recently discovered peptide that is the endogenous ligand for the orphan G-protein-coupled recepto...

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Autores principales: Peng-Fei Shan, Ying Lu, Rong-Rong Cui, Yi Jiang, Ling-Qing Yuan, Er-Yuan Liao
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Publicado: Public Library of Science (PLoS) 2011
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spelling oai:doaj.org-article:68493a50a4a348c38739a65ef50dbd002021-11-18T06:57:09ZApelin attenuates the osteoblastic differentiation of vascular smooth muscle cells.1932-620310.1371/journal.pone.0017938https://doaj.org/article/68493a50a4a348c38739a65ef50dbd002011-03-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21437254/?tool=EBIhttps://doaj.org/toc/1932-6203Vascular calcification, which results from a process osteoblastic differentiation of vascular smooth muscle cells (VSMCs), is a major risk factor for cardiovascular morbidity and mortality. Apelin is a recently discovered peptide that is the endogenous ligand for the orphan G-protein-coupled receptor, APJ. Several studies have identified the protective effects of apelin on the cardiovascular system. However, the effects and mechanisms of apelin on the osteoblastic differentiation of VSMCs have not been elucidated. Using a culture of calcifying vascular smooth muscle cells (CVMSCs) as a model for the study of vascular calcification, the relationship between apelin and the osteoblastic differentiation of VSMCs and the signal pathway involved were investigated. Alkaline phosphatase (ALP) activity and osteocalcin secretion were examined in CVSMCs. The involved signal pathway was studied using the extracellular signal-regulated kinase (ERK) inhibitor, PD98059, the phosphatidylinositol 3-kinase (PI3-K) inhibitor, LY294002, and APJ siRNA. The results showed that apelin inhibited ALP activity, osteocalcin secretion, and the formation of mineralized nodules. APJ protein was detected in CVSMCs, and apelin activated ERK and AKT (a downstream effector of PI3-K). Suppression of APJ with siRNA abolished the apelin-induced activation of ERK and Akt. Furthermore, inhibition of APJ expression, and the activation of ERK or PI3-K, reversed the effects of apelin on ALP activity. These results showed that apelin inhibited the osteoblastic differentiation of CVSMCs through the APJ/ERK and APJ/PI3-K/AKT signaling pathway. Apelin appears to play a protective role against arterial calcification.Peng-Fei ShanYing LuRong-Rong CuiYi JiangLing-Qing YuanEr-Yuan LiaoPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 3, p e17938 (2011)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Peng-Fei Shan
Ying Lu
Rong-Rong Cui
Yi Jiang
Ling-Qing Yuan
Er-Yuan Liao
Apelin attenuates the osteoblastic differentiation of vascular smooth muscle cells.
description Vascular calcification, which results from a process osteoblastic differentiation of vascular smooth muscle cells (VSMCs), is a major risk factor for cardiovascular morbidity and mortality. Apelin is a recently discovered peptide that is the endogenous ligand for the orphan G-protein-coupled receptor, APJ. Several studies have identified the protective effects of apelin on the cardiovascular system. However, the effects and mechanisms of apelin on the osteoblastic differentiation of VSMCs have not been elucidated. Using a culture of calcifying vascular smooth muscle cells (CVMSCs) as a model for the study of vascular calcification, the relationship between apelin and the osteoblastic differentiation of VSMCs and the signal pathway involved were investigated. Alkaline phosphatase (ALP) activity and osteocalcin secretion were examined in CVSMCs. The involved signal pathway was studied using the extracellular signal-regulated kinase (ERK) inhibitor, PD98059, the phosphatidylinositol 3-kinase (PI3-K) inhibitor, LY294002, and APJ siRNA. The results showed that apelin inhibited ALP activity, osteocalcin secretion, and the formation of mineralized nodules. APJ protein was detected in CVSMCs, and apelin activated ERK and AKT (a downstream effector of PI3-K). Suppression of APJ with siRNA abolished the apelin-induced activation of ERK and Akt. Furthermore, inhibition of APJ expression, and the activation of ERK or PI3-K, reversed the effects of apelin on ALP activity. These results showed that apelin inhibited the osteoblastic differentiation of CVSMCs through the APJ/ERK and APJ/PI3-K/AKT signaling pathway. Apelin appears to play a protective role against arterial calcification.
format article
author Peng-Fei Shan
Ying Lu
Rong-Rong Cui
Yi Jiang
Ling-Qing Yuan
Er-Yuan Liao
author_facet Peng-Fei Shan
Ying Lu
Rong-Rong Cui
Yi Jiang
Ling-Qing Yuan
Er-Yuan Liao
author_sort Peng-Fei Shan
title Apelin attenuates the osteoblastic differentiation of vascular smooth muscle cells.
title_short Apelin attenuates the osteoblastic differentiation of vascular smooth muscle cells.
title_full Apelin attenuates the osteoblastic differentiation of vascular smooth muscle cells.
title_fullStr Apelin attenuates the osteoblastic differentiation of vascular smooth muscle cells.
title_full_unstemmed Apelin attenuates the osteoblastic differentiation of vascular smooth muscle cells.
title_sort apelin attenuates the osteoblastic differentiation of vascular smooth muscle cells.
publisher Public Library of Science (PLoS)
publishDate 2011
url https://doaj.org/article/68493a50a4a348c38739a65ef50dbd00
work_keys_str_mv AT pengfeishan apelinattenuatestheosteoblasticdifferentiationofvascularsmoothmusclecells
AT yinglu apelinattenuatestheosteoblasticdifferentiationofvascularsmoothmusclecells
AT rongrongcui apelinattenuatestheosteoblasticdifferentiationofvascularsmoothmusclecells
AT yijiang apelinattenuatestheosteoblasticdifferentiationofvascularsmoothmusclecells
AT lingqingyuan apelinattenuatestheosteoblasticdifferentiationofvascularsmoothmusclecells
AT eryuanliao apelinattenuatestheosteoblasticdifferentiationofvascularsmoothmusclecells
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