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LncRNA MALAT1 Enhances ox-LDL-Induced Autophagy through the SIRT1/MAPK/NF-κB Pathway in Macrophages

Jiaqi Yang1, Xuze Lin1, Liangshan Wang2

  • 1Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China.

Current Vascular Pharmacology
|March 19, 2020
PubMed

Insights

Long-noncoding RNA MALAT1 promotes macrophage autophagy and cholesterol efflux in atherosclerosis by activating SIRT1, thereby inhibiting inflammatory pathways and reducing cell death.

Area of Science:

  • Molecular Biology
  • Cardiovascular Research
  • Cell Biology

Background:

  • Atherosclerosis pathogenesis involves macrophage apoptosis and inflammation, leading to necrotic core formation.
  • Oxidized low-density lipoprotein (ox-LDL) induces foam cell formation, a key event in atherosclerotic plaque development.
  • Long non-coding RNAs (lncRNAs) play crucial roles in regulating cellular processes relevant to disease.

Purpose of the Study:

  • To investigate the role of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in ox-LDL-induced macrophage responses.
  • To elucidate the molecular mechanisms by which MALAT1 influences autophagy, apoptosis, and inflammatory signaling in macrophages.

Main Methods:

  • Established an in vitro foam cell model using THP-1 derived macrophages incubated with ox-LDL.
  • Utilized quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and Western blot to assess gene and protein expression.
  • Employed small interfering RNA (siRNA) to knockdown MALAT1 and evaluate its functional impact on autophagy and apoptosis.

Main Results:

  • MALAT1 expression was upregulated in ox-LDL-induced foam cells, along with autophagy markers (LC-3, beclin-1).
  • Knockdown of MALAT1 significantly reduced autophagy activity and increased macrophage apoptosis.
  • MALAT1 was found to upregulate Sirtuin 1 (SIRT1), which subsequently inhibited MAPK and NF-κB signaling pathways.

Conclusions:

  • MALAT1 plays a protective role in the context of ox-LDL-induced macrophage injury by promoting autophagy and cholesterol efflux.
  • MALAT1 exerts its effects via the SIRT1/MAPK/NF-κB signaling axis, offering a potential therapeutic target for atherosclerosis.
Keywords:
AutophagyLC-3MALAT1MAPKNF-κBSIRT1macrophages

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