Abstract
BackgroundThe 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.MethodsTwenty 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.ResultsmiR-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).ConclusionsmiR-34a can inhibit the expression of PAI-1, thereby reducing urinary microalbumin content in hypertensive mice and protecting their renal function.
Highlights
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
The systolic blood pressure in the other groups was significantly increased, and there were no significant differences in systolic blood pressure among the other groups after treatment
The 24-h urinary microalbumin was increased in the other groups except miR-34a inhibitor + Si-PAI-1 group (P > 0.05)
Summary
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. Hypertension, with a high incidence, leads to renal function impairment. It has been confirmed that the urinary microalbumin content in patients with hypertension is abnormally elevated, which has been. The renal expression of plasminogen activator inhibitor (PAI-1) is abnormally elevated in hypertension-induced renal damage. Liu et al Eur J Med Res (2020) 25:3 the accumulation of extracellular matrix by inhibiting the degradation of extracellular matrix, thereby leading to glomerular sclerosis [7,8,9,10]. We found targeted binding sites for miR-34a and PAI-1 via the bioinformatics website. It was found that miR-34a is downregulated in pulmonary hypertension [13,14,15]. Silencing of miR-34a leads to further development of pulmonary hypertension
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