Open Access

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

  • Authors:
    • Zheng Gao
    • Li Wang
    • Jinyun Wang
    • Fengyong Yang
    • Jin Qu
  • View Affiliations

  • Published online on: August 3, 2017     https://doi.org/10.3892/etm.2017.4882
  • Pages: 2953-2959
  • Copyright: © Gao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

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<0.05). The results of luciferase assay indicated that miR‑181b directly targets TIMP3. The apoptosis rates of rat cardiomyocytes in the group transfected with miR‑181b or TIMP3 siRNA was significantly lower than the normal control group (P<0.05). miR‑181b may inhibit apoptosis of cardiomyocytes to protect myocardial cells through directly targeting TIMP3 genes, which serve important roles in HDCP.

Related Articles

Journal Cover

October-2017
Volume 14 Issue 4

Print ISSN: 1792-0981
Online ISSN:1792-1015

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Gao Z, Wang L, Wang J, Yang F and Qu J: Molecular mechanism of miR-181b in heart disease due to pregnancy-induced hypertension syndrome. Exp Ther Med 14: 2953-2959, 2017
APA
Gao, Z., Wang, L., Wang, J., Yang, F., & Qu, J. (2017). Molecular mechanism of miR-181b in heart disease due to pregnancy-induced hypertension syndrome. Experimental and Therapeutic Medicine, 14, 2953-2959. https://doi.org/10.3892/etm.2017.4882
MLA
Gao, Z., Wang, L., Wang, J., Yang, F., Qu, J."Molecular mechanism of miR-181b in heart disease due to pregnancy-induced hypertension syndrome". Experimental and Therapeutic Medicine 14.4 (2017): 2953-2959.
Chicago
Gao, Z., Wang, L., Wang, J., Yang, F., Qu, J."Molecular mechanism of miR-181b in heart disease due to pregnancy-induced hypertension syndrome". Experimental and Therapeutic Medicine 14, no. 4 (2017): 2953-2959. https://doi.org/10.3892/etm.2017.4882