ArticleEBioMedicine2018
Tissue-specific effects of targeted mutation of Mir29b1 in rats.
Article in EBioMedicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Dysregulation of miRNAs in Sicilian Patients with Autism Spectrum Disorder.Biomedicines · 2026Article
- Enterococcus faecalis: implications for host health.World journal of microbiology & biotechnology · 2024Review
- Renal lysophospholipase A1 contributes toiScience · 2022Article
- Broad-acting therapeutic effects of miR-29b-chitosan on hypertension and diabetic complications.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- β-Aminoisobutyric acid supplementation attenuated salt-sensitive hypertension in Dahl salt-sensitive rats through prevention of insufficient fumarase.Amino acids · 2022Article
- Role of the microRNA-29 family in myocardial fibrosis.Journal of physiology and biochemistry · 2021Review
- Inhibition of miRNA-29a regulates intestinal barrier function in diarrhea-predominant irritable bowel syndrome by upregulating ZO-1 and CLDN1.Experimental and therapeutic medicine · 2020Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundmiR-29 is a master regulator of extracellular matrix genes, but conflicting data on its anti-fibrotic effect have been reported. miR-29 improves nitric oxide (NO) production in arterioles by targeting Lypla1. Mir29b1 targeted mutation exacerbates hypertension in a model derived from the Dahl salt-sensitive rat. We examined the effect of Mir29b1 mutation on tissue fibrosis and NO levels with a focus on kidney regions.
methodsMir29b1 targeted mutant rats on the genetic background of SS-Chr13
findingsThe abundance of miR-29b and the co-transcribed miR-29a was substantially lower in mutant rats. Tissue fibrosis was significantly increased in the renal outer medulla, but not in the renal cortex, heart or liver in mutant rats on a 0.4% NaCl diet. Lypla1 protein abundance was significantly higher and NO levels lower in the renal outer medulla, but not in the renal cortex. After 14 days of a 4% NaCl diet, 24 h urine volume and urinary sodium excretion was significantly lower in mutant rats, and tissue fibrosis became higher in the heart. NO levels were lower in the renal outer medulla and heart, but not in the renal cortex. Human miR-29 genes are located in proximity with blood pressure-associated single nucleotide polymorphisms.
interpretationThe renal outer medulla might be particularly susceptible to the injurious effects of a miR-29 insufficiency, which might contribute to the development of hypertension in Mir29b1 mutant rats.
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