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Long non-coding RNA PCA3 inhibits lipid accumulation and atherosclerosis through the miR-140-5p/RFX7/ABCA1 axis

Zhen-Wang Zhao1, Min Zhang1, Ling-Xiao Liao2

  • 1Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, Hunan International Scientific and Technological Cooperation Base of Arteriosclerotic Disease, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.

Biochimica Et Biophysica Acta. Molecular and Cell Biology of Lipids
|February 12, 2021
PubMed
Abstract

Insights

Long noncoding RNA PCA3 inhibits atherosclerosis by promoting cholesterol efflux. PCA3 achieves this by interacting with miR-140-5p to increase RFX7 and ABCA1 expression in macrophages.

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • RNA Biology

Background:

  • Atherosclerosis is a chronic inflammatory disease characterized by lipid accumulation in macrophages.
  • Long noncoding RNAs (lncRNAs) play crucial roles in various biological processes, including cardiovascular diseases.
  • Prostate cancer antigen 3 (PCA3) is a lncRNA whose role in atherosclerosis remains largely unexplored.

Purpose of the Study:

  • To investigate the function of lncRNA PCA3 in the development of atherosclerosis.
  • To elucidate the molecular mechanism by which PCA3 influences macrophage lipid metabolism and reverse cholesterol transport.

Main Methods:

  • Utilized Gene Expression Omnibus (GEO) datasets to identify differentially expressed genes.
  • Quantified expression of PCA3, miR-140-5p, RFX7, and ABCA1 using qPCR and Western blotting in macrophage models.
  • Assessed macrophage lipid accumulation via Oil Red O staining and HPLC.
  • Validated molecular interactions using dual-luciferase reporter and chromatin immunoprecipitation assays.
  • Evaluated PCA3's effect on reverse cholesterol transport and atherosclerosis in an apoE knockout mouse model.

Main Results:

  • PCA3 expression was reduced in foam cells, while miR-140-5p was elevated.
  • PCA3 overexpression enhanced ABCA1-mediated cholesterol efflux and reduced lipid accumulation in macrophages.
  • RFX7 was identified as a key regulator binding to the ABCA1 promoter, increasing ABCA1 expression.
  • PCA3 was shown to upregulate RFX7 and ABCA1 expression by sponging miR-140-5p.
  • In vivo studies demonstrated that PCA3 promotes reverse cholesterol transport and inhibits atherosclerosis progression in apoE knockout mice.

Conclusions:

  • lncRNA PCA3 plays a protective role in atherosclerosis.
  • PCA3 promotes ABCA1-mediated cholesterol efflux, thereby inhibiting atherosclerosis.
  • The mechanism involves PCA3 sponging miR-140-5p and subsequently upregulating RFX7 and ABCA1 expression.
Keywords:
ABCA1AtherosclerosisLncRNA PCA3RFX7miR-140-5p

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