MiR155 modulates vascular calcification by regulating Akt-FOXO3a signalling and apoptosis in vascular smooth muscle cells.
Animals
Apoptosis
/ genetics
Cell Proliferation
/ genetics
Cells, Cultured
In Situ Nick-End Labeling
Mice
Mice, Inbred C57BL
MicroRNAs
/ genetics
Myocytes, Smooth Muscle
/ cytology
Phosphatidylinositol 3-Kinases
/ genetics
Phosphorylation
/ genetics
Proto-Oncogene Proteins c-akt
/ genetics
Real-Time Polymerase Chain Reaction
Signal Transduction
/ immunology
Akt
FOXO3a
apoptosis
microRNA-155
vascular calcification
vascular smooth muscle cell
Journal
Journal of cellular and molecular medicine
ISSN: 1582-4934
Titre abrégé: J Cell Mol Med
Pays: England
ID NLM: 101083777
Informations de publication
Date de publication:
01 2021
01 2021
Historique:
received:
19
06
2020
revised:
13
10
2020
accepted:
01
11
2020
pubmed:
20
11
2020
medline:
1
10
2021
entrez:
19
11
2020
Statut:
ppublish
Résumé
microRNA-155 (miR155) is pro-atherogenic; however, its role in vascular calcification is unknown. In this study, we aim to examine whether miR155 regulates vascular calcification and to understand the underlying mechanism. Quantitative real-time PCR showed that miR155 is highly expressed in human calcific carotid tissue and positively correlated with the expression of osteogenic genes. Wound-healing assay and TUNEL staining showed deletion of miR155 inhibited vascular smooth muscle cell (VSMC) migration and apoptosis. miR155 deficiency attenuated calcification of cultured mouse VSMCs and aortic rings induced by calcification medium, whereas miR155 overexpression promoted VSMC calcification. Compared with wild-type mice, miR155
Identifiants
pubmed: 33210462
doi: 10.1111/jcmm.16107
pmc: PMC7810936
doi:
Substances chimiques
MicroRNAs
0
Mirn155 microRNA, mouse
0
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
535-548Subventions
Organisme : NIH HHS
ID : HL145064
Pays : United States
Organisme : National Natural Science Foundation of China
ID : 81100162
Organisme : NIH HHS
ID : AT003961- 8455
Pays : United States
Organisme : NIH HHS
ID : HL116626
Pays : United States
Organisme : National Natural Science Foundation of China
ID : 81570247
Organisme : The Priority Academic Program Development of Jiangsu Higher Education Institutions
Organisme : Six Talent Peaks Project in Jiangsu Province
ID : 2015-WSN-29
Organisme : NHLBI NIH HHS
ID : R01 HL116626
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA218578
Pays : United States
Organisme : NCCIH NIH HHS
ID : P01 AT003961
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL145064
Pays : United States
Informations de copyright
© 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.
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