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Long noncoding RNA MALAT1 regulates apoptosis in ischemic stroke by sponging miR-205-3p and modulating PTEN

Qi Gao1, Yanfeng Wang1

  • 1Department of Neurology, The Affiliated Huaian No. 1 People's Hospital of Nanjing Medical University Huai'an 223300, Jiangsu, China.

American Journal of Translational Research
|July 14, 2020
PubMed

Insights

Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) may protect against ischemic stroke by suppressing apoptosis. This long non-coding RNA (lncRNA) regulates cell death via a competing endogenous RNA mechanism involving miR-205-3p and PTEN.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Ischemic stroke is a leading cause of global disability, involving complex pathological processes like apoptosis.
  • Long non-coding RNAs (lncRNAs), such as MALAT1, are implicated in regulating apoptosis, but their specific role in stroke remains unclear.

Purpose of the Study:

  • To investigate the cellular and molecular mechanisms of MALAT1 in an in vitro model of ischemic stroke.
  • To elucidate the relationship between MALAT1, miR-205-3p, and PTEN in OGD-induced apoptosis.

Main Methods:

  • Oxygen-glucose deprivation (OGD) model to induce apoptosis in vitro.
  • Quantitative analysis of MALAT1 and miR-205-3p expression.
  • MALAT1 knockdown experiments.
  • Assessment of cell viability and caspase-3 activation.
  • Analysis of competing endogenous RNA (ceRNA) interactions.

Main Results:

  • MALAT1 was found to be downregulated in OGD-induced apoptosis and correlated with miR-205-3p expression.
  • Knockdown of MALAT1 exacerbated OGD-induced apoptosis, reduced cell viability, and inhibited caspase-3 activation.
  • MALAT1 functions as a ceRNA for miR-205-3p, thereby regulating PTEN expression and protecting against OGD-induced apoptosis.

Conclusions:

  • MALAT1 plays a protective role by suppressing apoptosis in ischemic stroke.
  • MALAT1 acts as a ceRNA for miR-205-3p to modulate PTEN expression, offering a potential therapeutic target for ischemic stroke treatment.
Keywords:
LncRNAMALAT1PTENapoptosiscompeting endogenous RNAendothelial cellsischemic strokemiR-205-3p

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