RNA, Long Noncoding – ABC CARDIOL

ABC

Editorial

Long Non-Coding RNA, Apoptosis, and Doxorubicin-Induced Cardiotoxicity

Carolina R. Tonon et al. Bertha F. Polegato

Doxorubicin is one of the most effective chemotherapy drugs used in the treatment of many types of solid and hematologic malignancies. However, it causes several adverse effects. Cardiotoxicity is the most important collateral effect because it can lead to the development of heart failure, a chronic condition with high mortality, reaching with a 1-year risk of 15-30% and a 5-year risk of up to 75% in specific populations.

The pathophysiology of doxorubicin-induced cardiotoxicity is not completely understood. Classical pathways are involved such as direct damage to DNA, oxidative stress, inflammation, alteration in intracellular calcium transient, inhibition of muscle protein-related genes, mitochondrial dysfunction, and activation of cell death pathways, such as apoptosis. However, new mechanisms have gained more importance in the last decade, mainly in the genetic field.

[…]

Read Full Article

ABC

Original Article

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

Xiaoliang Han et al. Chao Li Qinjiong Ji Ling Zhang … Xiaofei Xie Huijuan Shang Hong Ye

Abstract

Background

It has been reported that solute carrier family 26 members 4 antisense RNA 1 (SLC26A4-AS1) is highly related to cardiac hypertrophy.

Objective

This research aims to investigate the role and specific mechanism of SLC26A4-AS1 in cardiac hypertrophy, providing a novel marker for cardiac hypertrophy treatment.

Methods

Angiotensin II (AngII) was infused into neonatal mouse ventricular cardiomyocytes (NMVCs) to induce cardiac hypertrophy. Gene expression was detected by quantitative real-time PCR (RT-qPCR). Protein levels were evaluated via western blot. Functional assays analyzed the role of SLC26A4-AS1. The mechanism of SLC26A4-AS1 was assessed by RNA-binding protein immunoprecipitation (RIP), RNA pull-down, and luciferase reporter assays. The P value <0.05 was identified as statistical significance. Student’s t-test evaluated the two-group comparison. The difference between different groups was analyzed by one-way analysis of variance (ANOVA).

Results

SLC26A4-AS1 is upregulated in AngII-treated NMVCs and promotes AngII-induced cardiac hypertrophy. SLC26A4-AS1 regulates its nearby gene solute carrier family 26 members 4 (SLC26A4) via functioning as a competing endogenous RNA (ceRNA) to modulate the microRNA (miR)-301a-3p and miR-301b-3p in NMVCs. SLC26A4-AS1 promotes AngII-induced cardiac hypertrophy via upregulating SLC26A4 or sponging miR-301a-3p/miR-301b-3p.

Conclusion

SLC26A4-AS1 aggravates AngII-induced cardiac hypertrophy via sponging miR-301a-3p or miR-301b-3p to enhance SLC26A4 expression.