Irisin suppresses PDGF-BB-induced proliferation of vascular smooth muscle cells <i>in vitro</i> by activating AMPK/mTOR-mediated autophagy

Restenosis is a pivotal factor that restricts the efficacy of coronary artery bypass grafting. Inhibition of vascular smooth muscle cells (VSMCs) proliferation can improve intimal hyperplasia and lumen stenosis. Irisin, a polypeptide secreted by muscle cells, has been demonstrated to have a protect...

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Main Authors: Fenqiang Qi, Yuxin Deng, Wei Huang, Yanli Cai, Kelin Hong, Shui Xiang
Format: Article
Language:English
Published: PAGEPress Publications 2024-10-01
Series:European Journal of Histochemistry
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Online Access:https://www.ejh.it/ejh/article/view/4104
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author Fenqiang Qi
Yuxin Deng
Wei Huang
Yanli Cai
Kelin Hong
Shui Xiang
author_facet Fenqiang Qi
Yuxin Deng
Wei Huang
Yanli Cai
Kelin Hong
Shui Xiang
author_sort Fenqiang Qi
collection DOAJ
description Restenosis is a pivotal factor that restricts the efficacy of coronary artery bypass grafting. Inhibition of vascular smooth muscle cells (VSMCs) proliferation can improve intimal hyperplasia and lumen stenosis. Irisin, a polypeptide secreted by muscle cells, has been demonstrated to have a protective role in various cardiovascular diseases. However, the effect and mechanism of irisin on VSMCs proliferation and phenotype switching remain unclear. Cell proliferation ability was assessed using the methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay and 5-ethynyl-2'-deoxyuridine (EdU) incorporation. Cell cycle analysis was performed using flow cytometry, while expression levels of contractile and synthesis-related proteins were determined through RT-qPCR and Western blot. The VSMCs were infected with an adenovirus carrying GFP-LC3, and the proportion of cells showing positive expression was assessed. Additionally, the formation of autophagic lysosomes in cells was observed through transmission electron microscopy. In this study, we have demonstrated the inhibitory effects of irisin on the proliferation and phenotypic transition of platelet-derived growth factor-BB (PDGF-BB)-induced VSMCs. More importantly, we have discovered that irisin can activate the AMP-activated protein kinase/mammalian target of rapamycin (AMPK/mTOR) signaling pathway to mediate autophagy in PDGF-BB-induced VSMCs. The inhibitory effect of irisin on PDGF-BB-induced VSMCs proliferation was significantly attenuated by the AMPK inhibitor, Compound C. Conversely the mTOR inhibitor, rapamycin further enhanced the inhibitory effect of irisin on PDGF-BB induced VSMCs proliferation. In conclusion, our findings suggest that irisin effectively suppresses the aberrant proliferation of VSMCs following PDGF-BB stimulation by modulating autophagy levels through the AMPK/mTOR signaling pathway.
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spelling doaj-art-7249dc26665e44fda35afbdd4726f1ab2025-08-20T01:47:37ZengPAGEPress PublicationsEuropean Journal of Histochemistry1121-760X2038-83062024-10-0168410.4081/ejh.2024.4104Irisin suppresses PDGF-BB-induced proliferation of vascular smooth muscle cells <i>in vitro</i> by activating AMPK/mTOR-mediated autophagyFenqiang Qi0Yuxin Deng1Wei Huang2Yanli Cai3Kelin Hong4Shui Xiang5Department of Cardiothoracic Surgery, Liuzhou Worker’s Hospital, LiuzhouDepartment of Cardiothoracic Surgery, Liuzhou Worker’s Hospital, LiuzhouDepartment of Cardiothoracic Surgery, Liuzhou Worker’s Hospital, LiuzhouDepartment of Cardiothoracic Surgery, The Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, EnshiDepartment of Cardiothoracic Surgery, The Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, EnshiDepartment of Cardiothoracic Surgery, Liuzhou Worker’s Hospital, Liuzhou; Department of Cardiothoracic Surgery, The Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Enshi Restenosis is a pivotal factor that restricts the efficacy of coronary artery bypass grafting. Inhibition of vascular smooth muscle cells (VSMCs) proliferation can improve intimal hyperplasia and lumen stenosis. Irisin, a polypeptide secreted by muscle cells, has been demonstrated to have a protective role in various cardiovascular diseases. However, the effect and mechanism of irisin on VSMCs proliferation and phenotype switching remain unclear. Cell proliferation ability was assessed using the methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay and 5-ethynyl-2'-deoxyuridine (EdU) incorporation. Cell cycle analysis was performed using flow cytometry, while expression levels of contractile and synthesis-related proteins were determined through RT-qPCR and Western blot. The VSMCs were infected with an adenovirus carrying GFP-LC3, and the proportion of cells showing positive expression was assessed. Additionally, the formation of autophagic lysosomes in cells was observed through transmission electron microscopy. In this study, we have demonstrated the inhibitory effects of irisin on the proliferation and phenotypic transition of platelet-derived growth factor-BB (PDGF-BB)-induced VSMCs. More importantly, we have discovered that irisin can activate the AMP-activated protein kinase/mammalian target of rapamycin (AMPK/mTOR) signaling pathway to mediate autophagy in PDGF-BB-induced VSMCs. The inhibitory effect of irisin on PDGF-BB-induced VSMCs proliferation was significantly attenuated by the AMPK inhibitor, Compound C. Conversely the mTOR inhibitor, rapamycin further enhanced the inhibitory effect of irisin on PDGF-BB induced VSMCs proliferation. In conclusion, our findings suggest that irisin effectively suppresses the aberrant proliferation of VSMCs following PDGF-BB stimulation by modulating autophagy levels through the AMPK/mTOR signaling pathway. https://www.ejh.it/ejh/article/view/4104Vascular smooth muscle cellsirisincell proliferationautophagyAMPK/mTOR signaling pathway
spellingShingle Fenqiang Qi
Yuxin Deng
Wei Huang
Yanli Cai
Kelin Hong
Shui Xiang
Irisin suppresses PDGF-BB-induced proliferation of vascular smooth muscle cells <i>in vitro</i> by activating AMPK/mTOR-mediated autophagy
European Journal of Histochemistry
Vascular smooth muscle cells
irisin
cell proliferation
autophagy
AMPK/mTOR signaling pathway
title Irisin suppresses PDGF-BB-induced proliferation of vascular smooth muscle cells <i>in vitro</i> by activating AMPK/mTOR-mediated autophagy
title_full Irisin suppresses PDGF-BB-induced proliferation of vascular smooth muscle cells <i>in vitro</i> by activating AMPK/mTOR-mediated autophagy
title_fullStr Irisin suppresses PDGF-BB-induced proliferation of vascular smooth muscle cells <i>in vitro</i> by activating AMPK/mTOR-mediated autophagy
title_full_unstemmed Irisin suppresses PDGF-BB-induced proliferation of vascular smooth muscle cells <i>in vitro</i> by activating AMPK/mTOR-mediated autophagy
title_short Irisin suppresses PDGF-BB-induced proliferation of vascular smooth muscle cells <i>in vitro</i> by activating AMPK/mTOR-mediated autophagy
title_sort irisin suppresses pdgf bb induced proliferation of vascular smooth muscle cells i in vitro i by activating ampk mtor mediated autophagy
topic Vascular smooth muscle cells
irisin
cell proliferation
autophagy
AMPK/mTOR signaling pathway
url https://www.ejh.it/ejh/article/view/4104
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AT yanlicai irisinsuppressespdgfbbinducedproliferationofvascularsmoothmusclecellsiinvitroibyactivatingampkmtormediatedautophagy
AT kelinhong irisinsuppressespdgfbbinducedproliferationofvascularsmoothmusclecellsiinvitroibyactivatingampkmtormediatedautophagy
AT shuixiang irisinsuppressespdgfbbinducedproliferationofvascularsmoothmusclecellsiinvitroibyactivatingampkmtormediatedautophagy