miR-34a targets PAI-1 to regulate urinary microalbumin and renal function in hypertensive mice

Abstract Background The aim of the study is to investigate the effects of miR-34a targeted at PAI-1 on urinary microalbumin and renal function in hypertensive mice. Methods Twenty specific-pathogen-free (SPF) BPN/3J mice were selected in normal group, and 120 SPF BPH/2J mice were evenly divided into...

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Main Authors: Ruitao Liu, Lihong Yang, Qingmin Wei
Format: Article
Language:English
Published: BMC 2020-03-01
Series:European Journal of Medical Research
Subjects:
Online Access:http://link.springer.com/article/10.1186/s40001-020-00404-7
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author Ruitao Liu
Lihong Yang
Qingmin Wei
author_facet Ruitao Liu
Lihong Yang
Qingmin Wei
author_sort Ruitao Liu
collection DOAJ
description Abstract Background The aim of the study is to investigate the effects of miR-34a targeted at PAI-1 on urinary microalbumin and renal function in hypertensive mice. Methods Twenty specific-pathogen-free (SPF) BPN/3J mice were selected in normal group, and 120 SPF BPH/2J mice were evenly divided into model group, negative control group, miR-34a mimic group, miR-34a inhibitor group, Si-PAI-1 group, and miR-34a inhibitor + Si-PAI-1 group. qRT-PCR was used to detect the expression of miR-34a and PAI-1 mRNA. The protein expressions of PAI-1, angiotensin-converting enzyme (ACE) and ACE2 were detected by Western blot. Serum levels of AngII and Ang1-7 were detected by ELISA. Results miR-34a negatively regulated the expression of PAI-1. Compared with the normal group, mice in the other groups had significantly lower body weight, increased systolic blood pressure and 24-h urinary microalbumin content, decreased miR-34a expression, superoxide dismutase (SOD) and nitric oxide (NO) content, and ACE2 protein expression, and increased PAI-1 expression, serum creatinine (Scr), blood urea nitrogen (BUN) malondialdehyde (MDA), AngII and Ang1-7 levels, and ACE protein expression (all P < 0.05). Compared with the model group, mice in the miR-34a mimic group and Si-PAI-1 group had no significant changes in body weight (all P > 0.05), while they had significantly lower systolic blood pressure and 24-h urinary microalbumin content, increased SOD and NO levels and ACE2 protein expression, and decreased PAI-1 expression, Scr, BUN, MDA, AngII and Ang1-7 levels, and ACE protein expression (all P < 0.05). Compared with the miR-34a inhibitor group, symptoms in miR-34a inhibitor + Si-PAI-1 group were significantly improved (all P < 0.05). Conclusions miR-34a can inhibit the expression of PAI-1, thereby reducing urinary microalbumin content in hypertensive mice and protecting their renal function.
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spelling doaj.art-5058c69c9b8842fc9b9d2b30fc4090be2022-12-21T23:54:39ZengBMCEuropean Journal of Medical Research2047-783X2020-03-012511910.1186/s40001-020-00404-7miR-34a targets PAI-1 to regulate urinary microalbumin and renal function in hypertensive miceRuitao Liu0Lihong Yang1Qingmin Wei2Department of Cardiovascular Medicine, Xingtai People’s HospitalDepartment of Cardiovascular Medicine, Xingtai People’s HospitalDepartment of Cardiovascular Medicine, Xingtai People’s HospitalAbstract Background The aim of the study is to investigate the effects of miR-34a targeted at PAI-1 on urinary microalbumin and renal function in hypertensive mice. Methods Twenty specific-pathogen-free (SPF) BPN/3J mice were selected in normal group, and 120 SPF BPH/2J mice were evenly divided into model group, negative control group, miR-34a mimic group, miR-34a inhibitor group, Si-PAI-1 group, and miR-34a inhibitor + Si-PAI-1 group. qRT-PCR was used to detect the expression of miR-34a and PAI-1 mRNA. The protein expressions of PAI-1, angiotensin-converting enzyme (ACE) and ACE2 were detected by Western blot. Serum levels of AngII and Ang1-7 were detected by ELISA. Results miR-34a negatively regulated the expression of PAI-1. Compared with the normal group, mice in the other groups had significantly lower body weight, increased systolic blood pressure and 24-h urinary microalbumin content, decreased miR-34a expression, superoxide dismutase (SOD) and nitric oxide (NO) content, and ACE2 protein expression, and increased PAI-1 expression, serum creatinine (Scr), blood urea nitrogen (BUN) malondialdehyde (MDA), AngII and Ang1-7 levels, and ACE protein expression (all P < 0.05). Compared with the model group, mice in the miR-34a mimic group and Si-PAI-1 group had no significant changes in body weight (all P > 0.05), while they had significantly lower systolic blood pressure and 24-h urinary microalbumin content, increased SOD and NO levels and ACE2 protein expression, and decreased PAI-1 expression, Scr, BUN, MDA, AngII and Ang1-7 levels, and ACE protein expression (all P < 0.05). Compared with the miR-34a inhibitor group, symptoms in miR-34a inhibitor + Si-PAI-1 group were significantly improved (all P < 0.05). Conclusions miR-34a can inhibit the expression of PAI-1, thereby reducing urinary microalbumin content in hypertensive mice and protecting their renal function.http://link.springer.com/article/10.1186/s40001-020-00404-7miR-34aPAI-1HypertensionUrinary microalbuminRenal function
spellingShingle Ruitao Liu
Lihong Yang
Qingmin Wei
miR-34a targets PAI-1 to regulate urinary microalbumin and renal function in hypertensive mice
European Journal of Medical Research
miR-34a
PAI-1
Hypertension
Urinary microalbumin
Renal function
title miR-34a targets PAI-1 to regulate urinary microalbumin and renal function in hypertensive mice
title_full miR-34a targets PAI-1 to regulate urinary microalbumin and renal function in hypertensive mice
title_fullStr miR-34a targets PAI-1 to regulate urinary microalbumin and renal function in hypertensive mice
title_full_unstemmed miR-34a targets PAI-1 to regulate urinary microalbumin and renal function in hypertensive mice
title_short miR-34a targets PAI-1 to regulate urinary microalbumin and renal function in hypertensive mice
title_sort mir 34a targets pai 1 to regulate urinary microalbumin and renal function in hypertensive mice
topic miR-34a
PAI-1
Hypertension
Urinary microalbumin
Renal function
url http://link.springer.com/article/10.1186/s40001-020-00404-7
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AT lihongyang mir34atargetspai1toregulateurinarymicroalbuminandrenalfunctioninhypertensivemice
AT qingminwei mir34atargetspai1toregulateurinarymicroalbuminandrenalfunctioninhypertensivemice