miR32-5p promoted vascular smooth muscle cell calcification by upregulating TNFα in the microenvironment

Abstract Background Vascular calcification is often associated with chronic inflammation and is a risk factor for brain arterial stiffness. Our previous results showed that miR32-5p was positively correlated with vascular smooth muscle cells (VSMC) calcification, but it is unclear whether miR32-5p p...

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Main Authors: Jingsong Cao, Ling Chen, Xiaoling Zhong, Yingying Shen, Yan Gao, Qian Chen, Xuyu Zu, Jianghua Liu
Format: Article
Language:English
Published: BMC 2020-01-01
Series:BMC Immunology
Subjects:
Online Access:https://doi.org/10.1186/s12865-019-0324-x
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author Jingsong Cao
Ling Chen
Xiaoling Zhong
Yingying Shen
Yan Gao
Qian Chen
Xuyu Zu
Jianghua Liu
author_facet Jingsong Cao
Ling Chen
Xiaoling Zhong
Yingying Shen
Yan Gao
Qian Chen
Xuyu Zu
Jianghua Liu
author_sort Jingsong Cao
collection DOAJ
description Abstract Background Vascular calcification is often associated with chronic inflammation and is a risk factor for brain arterial stiffness. Our previous results showed that miR32-5p was positively correlated with vascular smooth muscle cells (VSMC) calcification, but it is unclear whether miR32-5p promoted VSMC calcification by regulating inflammatory factor production. Results In this study, bioinformatics analysis was used to select tumour necrosis factor α (TNFα) as a candidate inflammatory factor associated with calcification. Moreover, alizarin red staining and qRT-PCR analysis revealed that TNFα produced by BV2 cells was the key promoting factor of VSMC calcification. Interestingly, the expression of TNFα was significantly increased at the mRNA and protein levels after miR32-5p mimic treatment but significantly decreased after miR32-5p antagomir treatment. To explore the mechanism of the regulation of TNFα expression by miR32-5p, bioinformatics analysis indicated that PIKfyve was a candidate target gene of miR32-5p, and luciferase assays verified that the expression of PIKfyve was significantly repressed by miR32-5p mimics. Importantly, rescue experiments showed that the expression of TNFα in BV2 cells treated with miR32-5p antagomir and the PIKfyve inhibitor YM201636 was significantly increased. Conclusions The production of TNFα in microglia could be affected by miR32-5p targeting PIKfyve, and these results will be beneficial to reveal the mechanism of brain arterial calcification.
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spelling doaj.art-3d6f5fdd649f491e98708407bdf68a6f2022-12-21T22:26:11ZengBMCBMC Immunology1471-21722020-01-012111810.1186/s12865-019-0324-xmiR32-5p promoted vascular smooth muscle cell calcification by upregulating TNFα in the microenvironmentJingsong Cao0Ling Chen1Xiaoling Zhong2Yingying Shen3Yan Gao4Qian Chen5Xuyu Zu6Jianghua Liu7Institute of Clinical Medicine, The First Affiliated Hospital of University of South ChinaInstitute of Clinical Medicine, The First Affiliated Hospital of University of South ChinaInstitute of Clinical Medicine, The First Affiliated Hospital of University of South ChinaInstitute of Clinical Medicine, The First Affiliated Hospital of University of South ChinaInstitute of Clinical Medicine, The First Affiliated Hospital of University of South ChinaInstitute of Clinical Medicine, The First Affiliated Hospital of University of South ChinaInstitute of Clinical Medicine, The First Affiliated Hospital of University of South ChinaInstitute of Clinical Medicine, The First Affiliated Hospital of University of South ChinaAbstract Background Vascular calcification is often associated with chronic inflammation and is a risk factor for brain arterial stiffness. Our previous results showed that miR32-5p was positively correlated with vascular smooth muscle cells (VSMC) calcification, but it is unclear whether miR32-5p promoted VSMC calcification by regulating inflammatory factor production. Results In this study, bioinformatics analysis was used to select tumour necrosis factor α (TNFα) as a candidate inflammatory factor associated with calcification. Moreover, alizarin red staining and qRT-PCR analysis revealed that TNFα produced by BV2 cells was the key promoting factor of VSMC calcification. Interestingly, the expression of TNFα was significantly increased at the mRNA and protein levels after miR32-5p mimic treatment but significantly decreased after miR32-5p antagomir treatment. To explore the mechanism of the regulation of TNFα expression by miR32-5p, bioinformatics analysis indicated that PIKfyve was a candidate target gene of miR32-5p, and luciferase assays verified that the expression of PIKfyve was significantly repressed by miR32-5p mimics. Importantly, rescue experiments showed that the expression of TNFα in BV2 cells treated with miR32-5p antagomir and the PIKfyve inhibitor YM201636 was significantly increased. Conclusions The production of TNFα in microglia could be affected by miR32-5p targeting PIKfyve, and these results will be beneficial to reveal the mechanism of brain arterial calcification.https://doi.org/10.1186/s12865-019-0324-xVSMC calcificationmiR32-5pPIKfyveTNFαMicroenvironment
spellingShingle Jingsong Cao
Ling Chen
Xiaoling Zhong
Yingying Shen
Yan Gao
Qian Chen
Xuyu Zu
Jianghua Liu
miR32-5p promoted vascular smooth muscle cell calcification by upregulating TNFα in the microenvironment
BMC Immunology
VSMC calcification
miR32-5p
PIKfyve
TNFα
Microenvironment
title miR32-5p promoted vascular smooth muscle cell calcification by upregulating TNFα in the microenvironment
title_full miR32-5p promoted vascular smooth muscle cell calcification by upregulating TNFα in the microenvironment
title_fullStr miR32-5p promoted vascular smooth muscle cell calcification by upregulating TNFα in the microenvironment
title_full_unstemmed miR32-5p promoted vascular smooth muscle cell calcification by upregulating TNFα in the microenvironment
title_short miR32-5p promoted vascular smooth muscle cell calcification by upregulating TNFα in the microenvironment
title_sort mir32 5p promoted vascular smooth muscle cell calcification by upregulating tnfα in the microenvironment
topic VSMC calcification
miR32-5p
PIKfyve
TNFα
Microenvironment
url https://doi.org/10.1186/s12865-019-0324-x
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