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SLC26A4-AS1 Aggravates AngII-induced Cardiac Hypertrophy by Enhancing SLC26A4 Expression

Xiaoliang Han1, Chao Li2, Qinjiong Ji1

  • 1Departamento de Cardiologia, Anhui Provincial Chest Hospital, (Instituto de Controle de Tuberculose de Anhui), Hefei, Anhui - China.

Arquivos Brasileiros De Cardiologia
|April 26, 2023
PubMed

Insights

Solute carrier family 26 members 4 antisense RNA 1 (SLC26A4-AS1) promotes cardiac hypertrophy by upregulating SLC26A4. This study reveals SLC26A4-AS1 as a potential therapeutic target for cardiac hypertrophy.

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • Genetics

Background:

  • Solute carrier family 26 members 4 antisense RNA 1 (SLC26A4-AS1) has been linked to cardiac hypertrophy.
  • Understanding the precise role of SLC26A4-AS1 in this condition is crucial.

Purpose of the Study:

  • To investigate the role and mechanism of SLC26A4-AS1 in Angiotensin II-induced cardiac hypertrophy.
  • To identify SLC26A4-AS1 as a potential therapeutic marker for cardiac hypertrophy.

Main Methods:

  • Neonatal mouse ventricular cardiomyocytes (NMVCs) were treated with Angiotensin II (AngII) to induce hypertrophy.
  • Gene expression (RT-qPCR) and protein levels (Western blot) were analyzed.
  • Mechanism explored using RNA immunoprecipitation, RNA pull-down, and luciferase assays.

Main Results:

  • SLC26A4-AS1 was upregulated in AngII-treated NMVCs, promoting cardiac hypertrophy.
  • SLC26A4-AS1 acts as a competing endogenous RNA (ceRNA), modulating miR-301a-3p and miR-301b-3p.
  • It enhances SLC26A4 expression, contributing to hypertrophy.

Conclusions:

  • SLC26A4-AS1 exacerbates AngII-induced cardiac hypertrophy.
  • This occurs by sponging miR-301a-3p/miR-301b-3p, leading to increased SLC26A4 expression.
Abstract

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