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miR-34a targets PAI-1 to regulate urinary microalbumin and renal function in hypertensive mice
Ruitao Liu1, Lihong Yang1, Qingmin Wei2
1Department of Cardiovascular Medicine, Xingtai People's Hospital, No.16 Hongxing East Street, Qiaodong District, Xingtai, 054000, Hebei, China.
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.
Insights
MicroRNA-34a (miR-34a) targets PAI-1 to reduce urinary microalbumin and protect kidney function in hypertensive mice. This study highlights miR-34a as a potential therapeutic target for hypertension-related kidney disease.
Area of Science:
- Molecular Biology
- Nephrology
- Genetics
Background:
- Hypertension is a major risk factor for chronic kidney disease.
- Microalbuminuria is an early indicator of kidney damage in hypertensive individuals.
- The role of microRNA-34a (miR-34a) and its target PAI-1 in hypertensive nephropathy requires further investigation.
Purpose of the Study:
- To investigate the effects of miR-34a targeting PAI-1 on urinary microalbumin and renal function in a mouse model of hypertension.
- To elucidate the molecular mechanisms underlying miR-34a-mediated regulation of PAI-1 and its impact on renal parameters.
Main Methods:
- Establishment of a hypertensive mouse model.
- Intervention with miR-34a mimic, miR-34a inhibitor, and Si-PAI-1.
- Quantitative real-time PCR (qRT-PCR) for gene expression analysis.
- Western blot for protein expression analysis of PAI-1, ACE, and ACE2.
- Enzyme-linked immunosorbent assay (ELISA) for serum AngII and Ang1-7 levels.
Main Results:
- miR-34a was found to negatively regulate PAI-1 expression.
- Hypertensive mice exhibited decreased miR-34a, increased PAI-1, elevated blood pressure, and increased urinary microalbumin.
- Administration of miR-34a mimic or Si-PAI-1 improved renal function markers, reduced PAI-1, and normalized blood pressure and microalbuminuria.
- Combined inhibition of miR-34a and PAI-1 showed improved outcomes compared to miR-34a inhibitor alone.
Conclusions:
- miR-34a plays a protective role in hypertensive nephropathy by inhibiting PAI-1 expression.
- Targeting miR-34a offers a potential therapeutic strategy for reducing microalbuminuria and preserving renal function in hypertension.
- The miR-34a/PAI-1 axis is a critical regulator of kidney damage in hypertensive conditions.
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