Molecular mechanism of miR-181b in heart disease due to pregnancy-induced hypertension syndrome

The present study aimed to investigate the molecular mechanisms of microRNA (miR)-181b in heart disease due to hypertensive disorders complicating pregnancy (HDCP) through regulating the expression of metallopeptidase inhibitor 3 (TIMP3). miR-181b expression was detected by reverse transcription-qua...

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Bibliographic Details
Published in:Experimental and therapeutic medicine 2017-10, Vol.14 (4), p.2953-2959
Main Authors: Gao, Zheng, Wang, Li, Wang, Jinyun, Yang, Fengyong, Qu, Jin
Format: Article
Language:English
Subjects:
Age
Apoptosis
Cardiovascular disease
Chinese medicine
Heart
Hospitals
Hypertension
Hypoxia
Laboratory animals
Patients
Pregnancy
Studies
Womens health
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Summary:The present study aimed to investigate the molecular mechanisms of microRNA (miR)-181b in heart disease due to hypertensive disorders complicating pregnancy (HDCP) through regulating the expression of metallopeptidase inhibitor 3 (TIMP3). miR-181b expression was detected by reverse transcription-quantitative polymerase chain reaction in peripheral blood samples from patients with HDCP. These samples were analyzed for clinical pathological characteristics. The primary cardiomyocytes of rats were cultured in hypoxic conditions for 24 h, in which miR-181b expression was detected at different time points. The expression of TIMP3 was assessed in normal rat cardiomyocytes following transfection with miR-181b mimics by western blot analysis. The TIMP3 protein was also detected in cardiomyocytes following transfection with TIMP3 short interfering-RNA. The apoptosis rate of transfected cardiomyocytes was detected by flow cytometry following 24 h of culture in a hypoxic environment. Luciferase assay was applied to validate whether miR-181b binds to the 3' untranslated region of TIMP3 mRNA. miR-181b expression was significantly downregulated in the peripheral blood of patients with HDCP and the miR-181b expression was negatively associated with the grades of hypertension (P
ISSN:1792-0981
1792-1015
DOI:10.3892/etm.2017.4882