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RNA Pull-down Procedure to Identify RNA Targets of a Long Non-coding RNA
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RNA Pull-down Procedure to Identify RNA Targets of a Long Non-coding RNA

Published on: April 10, 2018

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Long non-coding RNA cytoskeleton regulator RNA (CYTOR) modulates pathological cardiac hypertrophy through

Yuan Yuan1, Juan Wang2, Qiuxiang Chen3

  • 1Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute of Wuhan University, Hubei Key Laboratory of Cardiology, Wuhan 430060, China.

Biochimica Et Biophysica Acta. Molecular Basis of Disease
|February 23, 2019
PubMed

Insights

Long non-coding RNA CYTOR may protect against cardiac hypertrophy by regulating miR-155, IKKi, and NF-kB signaling. CYTOR acts as a ceRNA, counteracting miR-155

Area of Science:

  • Molecular Biology
  • Cardiovascular Research
  • Non-coding RNA Biology

Background:

  • Pathological cardiac hypertrophy can lead to heart failure and sudden death.
  • Previous studies linked IKKi deficiency to cardiac hypertrophy via AKT and NF-kB pathways.
  • Non-coding RNAs, including lncRNAs and miRNAs, are critical in pathological processes.

Purpose of the Study:

  • Identify upregulated long non-coding RNAs (lncRNAs) in cardiac hypertrophy.
  • Investigate the role of lncRNA cytoskeleton regulator RNA (CYTOR) in cardiac hypertrophy.
  • Elucidate the mechanism of CYTOR action, focusing on its interaction with miR-155 and IKBKE.

Main Methods:

  • Microarray analysis of GEO database for lncRNA identification.
  • Analysis of GTEx project data for CYTOR-IKBKE correlation.
  • Experimental manipulation of CYTOR and miR-155 in mouse models and cardiomyocytes.
  • Luciferase reporter and RNA immunoprecipitation (RIP) assays to confirm interactions.

Main Results:

  • CYTOR was upregulated in cardiac hypertrophy and positively correlated with IKBKE.
  • CYTOR knockdown exacerbated cardiac hypertrophy induced by aortic banding and Angiotensin II.
  • CYTOR functions as a competing endogenous RNA (ceRNA) for miR-155, preventing miR-155-mediated repression of IKBKE.
  • CYTOR knockdown decreased IKKi protein and activated NF-kB, effects partially rescued by miR-155 inhibition.

Conclusions:

  • CYTOR plays a protective role in cardiac hypertrophy.
  • The protective mechanism involves CYTOR acting as a ceRNA for miR-155 to regulate IKBKE and downstream NF-kB signaling.
  • CYTOR represents a potential therapeutic target for managing cardiac hypertrophy.

Keywords:
Cardiac hypertrophyIKBKENF-κB signalinglncRNA CYTORmiR-155

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