MicroRNA-183-5p acts as a potential diagnostic biomarker for atherosclerosis and regulates the growth of vascular smooth muscle cell

Abstract Background Atherosclerosis (AS) is a multifactorial chronic disease, and vascular smooth muscle cells (VSMCs) plays an important role in the pathology of AS. MicroRNAs regulate multiple cellular biological processes. This study aimed to investigate the clinical value of miR-183-5p in AS patients, and further explored the effects of miR-183-5p on the proliferation and migration of VSMCs. Methods qRT-PCR was used to test the level of miR-183-5p. The diagnostic value of miR-183-5p for AS patients was assessed by a receiver operating characteristic (ROC) analysis. Cell proliferation and migration were determined via CCK-8 and Transwell assay. Results MiR-183-5p was highly expressed in AS patients compared with the healthy group. Serum miR-183-5p expression was positively associated with CIMT and CRP in AS patients. The ROC analysis suggested that miR-183-5p had quality to be used as a biomarker with high specificity and sensitivity for AS detection. Overexpression of miR-183-5p promoted the proliferation and migration of VSMCs. Downregulation of miR-183-5p attenuated ox-LDL stimulated VSMCs proliferation and migration. Conclusion MiR-183-5p is highly expressed in AS patients, and downregulation of miR-183-5p attenuated ox-LDL stimulated VSMCs proliferation and migration. MiR-183-5p may be a key molecular for the diagnosis and treatment of AS in the future.

MicroRNA-183-5p acts as a potential diagnostic biomarker for atherosclerosis and regulates the growth of vascular smooth muscle cell

10.21203/rs.2.14613/v1 ◽

2019 ◽

Author(s):

Bin Sun ◽

Zhengkun Shan ◽

Guoyu Sun ◽

Xiaolong Wang

Keyword(s):

Cell Proliferation ◽

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Roc Analysis ◽

High Specificity ◽

Clinical Value ◽

Cell Proliferation And Migration ◽

Specificity And Sensitivity ◽

And Migration ◽

Abstract Background: Atherosclerosis (AS) is a multifactorial chronic disease, and vascular smooth muscle cells (VSMCs) plays an important role in the pathology of AS. MicroRNAs regulate multiple cellular biological processes. This study aimed to investigate the clinical value of miR-183-5p in AS patients, and further explored the effects of miR-183-5p on the proliferation and migration of VSMCs.Methods: qRT-PCR was used to test the level of miR-183-5p. The diagnostic value of miR-183-5p for AS patients was assessed by a receiver operating characteristic (ROC) analysis. Cell proliferation and migration were determined via CCK-8 and Transwell assay.Results: MiR-183-5p was highly expressed in AS patients compared with the healthy group. Serum miR-183-5p expression was positively associated with CIMT and CRP in AS patients. The ROC analysis suggested that miR-183-5p had quality to be used as a biomarker with high specificity and sensitivity for AS detection. Overexpression of miR-183-5p promoted the proliferation and migration of VSMCs.Conclusion: MiR-183-5p is highly expressed in AS patients, and overexpression of miR-183-5p promots the cell proliferation and migration of VSMCs. MiR-183-5p may be a key molecular for the diagnosis and treatment of AS in the future.

MiR-455-5p serves as a biomarker of atherosclerosis and inhibits vascular smooth muscle cell proliferation and migration

Personalized Medicine ◽

10.2217/pme-2020-0136 ◽

2021 ◽

Author(s):

Xiang Zhang ◽

Yan Liu ◽

Jing Zhao ◽

Tingguo Yan

Keyword(s):

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Diagnostic Value ◽

Luciferase Reporter ◽

Luciferase Reporter Gene ◽

Clinical Value ◽

Gene Assay ◽

And Migration ◽

Clinical Experiments ◽

Background: This study discussed the clinical value and expression level of miR-455-5p in atherosclerosis (AS) patients. Meanwhile, its regulatory effect on the proliferation and migration of vascular smooth muscle cells (VSMCs) was further analyzed. Materials & methods: Clinical experiments were detected by quantitative real-time PCR and receiver operating characteristic. Cell experiments were detected by CCK-8, transwell and luciferase reporter gene assay. Results: miR-455-5p was low expressed in AS patients and had diagnostic value to distinguish AS patients from healthy controls. MiR-455-5p inhibited the proliferation and migration of VSMCs. SOCS3 was the target gene of miR-455-5p. Conclusion: MiR-455-5p may be used as a potential diagnostic biomarker for AS. MiR-455-5p may inhibit the proliferation and migration of VSMCs through targeting SOCS3.

miR‐141‐5p suppresses vascular smooth muscle cell inflammation, proliferation, and migration via inhibiting the HMGB1/NF‐κB pathway

Journal of Biochemical and Molecular Toxicology ◽

10.1002/jbt.22828 ◽

2021 ◽

Author(s):

Yadong Li ◽

Haide Li ◽

Bin Chen ◽

Fan Yang ◽

Zhiying Hao

Keyword(s):

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Smooth Muscle Cell ◽

Muscle Cell ◽

And Migration ◽

Ginkolide A-Gold Nanoparticles Inhibit Vascular Smooth Muscle Proliferation And Migration In Vitro And Reduces Intimal Hyperplasia In A Mouse Model

Journal of Surgical Research ◽

10.1016/j.jss.2010.11.481 ◽

2011 ◽

Vol 165 (2) ◽

pp. 253-254

Author(s):

S.M. Weakley ◽

X. Wang ◽

H. Mu ◽

P.H. Lin ◽

Q. Yao ◽

...

Keyword(s):

Gold Nanoparticles ◽

Smooth Muscle ◽

Mouse Model ◽

Vascular Smooth Muscle ◽

Intimal Hyperplasia ◽

Smooth Muscle Proliferation ◽

And Migration ◽

MiR-147b influences vascular smooth muscle cell proliferation and migration via targeting YY1 and modulating Wnt/β-catenin activities

Acta Biochimica et Biophysica Sinica ◽

10.1093/abbs/gmy086 ◽

2018 ◽

Vol 50 (9) ◽

pp. 905-913 ◽

Cited By ~ 8

Author(s):

Yulun Yue ◽

Wenyan Lv ◽

Lin Zhang ◽

Wei Kang

Keyword(s):

Cell Proliferation ◽

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Smooth Muscle Cell ◽

Muscle Cell ◽

Smooth Muscle Cell Proliferation ◽

Cell Proliferation And Migration ◽

And Migration ◽

Extract of Oxytropis pseudoglandulosa inhibits vascular smooth muscle cell proliferation and migration via suppression of ERK1/2 and Akt signaling pathways1

Clinical Hemorheology and Microcirculation ◽

10.3233/ch-189126 ◽

2018 ◽

Vol 69 (1-2) ◽

pp. 277-287 ◽

Cited By ~ 1

Author(s):

Jiyun Lee ◽

Chang Youn Lee ◽

Hyang-Hee Seo ◽

Badamtsetseg Bazarragchaa ◽

Gantuya Batdelger ◽

...

Keyword(s):

Cell Proliferation ◽

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Smooth Muscle Cell ◽

Muscle Cell ◽

Akt Signaling ◽

Cell Proliferation And Migration ◽

And Migration ◽

Abstract 239: Olfactomedin 2 Regulates Vascular Smooth Muscle Cell Phenotypic Modulation by Mediating the Interaction Between Runx2 and SRF

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvb.35.suppl_1.239 ◽

2015 ◽

Vol 35 (suppl_1) ◽

Author(s):

Ning Shi ◽

Xiao-Bing Cui ◽

Shi-You Chen

Keyword(s):

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Smooth Muscle Cell ◽

Muscle Cell ◽

Marker Genes ◽

Important Process ◽

Phenotypic Modulation ◽

And Migration ◽

Olfactomedin 2 (Olfm2) is a novel regulator for vascular smooth muscle cell (SMC) differentiation, but it is unclear whether Olfm2 is also involved in SMC phenotypic modulation, an important process associated with vascular injury. In this study, we found that Olfm2 was induced during PDGF-BB-induced SMC phenotypic modulation. Olfm2 knockdown attenuated PDGF-BB-induced suppression of SM marker genes including SM myosin heavy chain and SM22α, and also inhibited PDGF-BB-stimulated SMC proliferation and migration. On the other hand, Olfm2 overexpression down-regulated SM markers gene expression, and promoted SMC proliferation marker PCNA expression. Moreover, PDGF-BB slightly induced expression of Runx2, which interfered with the formation of SRF/myocardin ternary complex, but dramatically enhanced SRF-Runx2 interaction, suggesting that certain factors mediate SRF-Runx2 interaction. Indeed, Olfm2 physically interacted with both SRF and Runx2. Blockade of Olfm2 inhibited SRF association with Runx2, leading to increased association between SRF and myocardin, which in turn activated the transcription of SM markers, whereas overexpression of Olfm2 promoted SRF binding to Runx2. These results demonstrated that Olfm2 mediates the interaction between SRF and Runx2, contributing to SMC phenotypic modulation.