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MicroRNA (miRNA) are short, regulatory RNA transcribed from introns—non-coding regions of a gene—or intergenic regions—stretches of DNA present between genes. Several processing steps are required to form biologically active, mature miRNA. The initial transcript, called primary miRNA (pri-mRNA), base-pairs with itself forming a stem-loop structure. Within the nucleus, an endonuclease enzyme, called Drosha, shortens the stem-loop structure into hairpin-shaped pre-miRNA. After...
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Gene expression can be regulated at almost every step from gene to protein. Transcription is the step that is most commonly regulated. This involves the binding of proteins to short regulatory sequences on the DNA. This association can either promote or inhibit the transcription of a gene associated with the respective sequence.
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Alteration in microRNA-25 expression regulate cardiac function via renin secretion.

Hongzhi Li1, Yeming Xie2, Yunshuang Liu3

  • 1Jilin Provincial Key Laboratory of Animal Embryo Engineering, Department of Animal Biotechnology, College of Animal Science, Jilin University, Changchun 130062, China; Department of Toxicology, School of Public Health, Beihua University, Jilin 132011, Jilin, China; Heilongjiang Key Laboratory of Anti-Fibrosis Biotherapy and Hong Qi Hospital, Mudanjiang Medical University, Mudanjiang 157011, China.

Experimental Cell Research
|March 3, 2018
PubMed
Summary

MicroRNA-25 (miR-25) levels initially decrease in heart failure but rise in end-stage disease, impacting cardiac function and blood pressure. This study reveals miR-25

Keywords:
Blood pressureFibrosisHeart failureRASmicroRNA

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Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Biomarker Discovery

Background:

  • Heart failure (HF) stems from various cardiovascular conditions, yet specific microRNA (miRNA) involvement is not fully understood.
  • MicroRNAs are small non-coding RNAs that regulate gene expression and are implicated in cardiovascular disease pathogenesis.
  • Identifying novel biomarkers and therapeutic targets for HF is crucial for improving patient outcomes.

Purpose of the Study:

  • To investigate the expression patterns of miR-25 in different stages of heart disease.
  • To elucidate the functional role of miR-25 in cardiac fibrosis, apoptosis, and blood pressure regulation.
  • To explore the potential of miR-25 as a biomarker for heart failure progression.

Main Methods:

  • Quantitative PCR (q-PCR) to measure miR-25 expression in human blood samples from healthy individuals and patients with dilated cardiomyopathy, remote infarct, hypertensive heart disease, and heart failure.
  • In vivo studies using normal mice with miR-25 overexpression and inhibition, and miR-25 cluster knockout mice.
  • RNA sequencing to identify miR-25 target genes.
  • In vitro luciferase reporter assays to validate miR-25 targets (Pde3a and Cacnalc).

Main Results:

  • miR-25 expression decreased at the onset of heart failure but increased in end-stage disease.
  • Overexpression of miR-25 in mice induced cardiomyocyte fibrosis and apoptosis.
  • Inhibition of miR-25 activated the renin-angiotensin system (RAS), leading to high blood pressure and mild cardiac dilation.
  • miR-25 cluster knockout mice exhibited high blood pressure without significant cardiac dysfunction.
  • RNA sequencing revealed alterations in miR-25 target genes, including those related to renin secretion.

Conclusions:

  • miR-25 exhibits dynamic expression changes throughout the progression of heart disease.
  • miR-25 plays a complex role in regulating cardiac structure, function, and blood pressure.
  • These findings offer a new perspective on miR-25's function in heart failure and its potential as a diagnostic or therapeutic target.