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Long non-coding RNA MALAT1 regulates cardiomyocytes apoptosis after hypoxia/reperfusion injury via modulating

Rongguo Sun1, Liang Zhang2

  • 1NO.3 Department of Internal Medicine Cardiovascular, Cangzhou Central Hospital, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|March 8, 2019
PubMed

Insights

Long non-coding RNA MALAT1 and PDCD4 are upregulated in myocardial infarction. MALAT1 acts as a ceRNA for miR-200a-3p, upregulating PDCD4 and impacting cell proliferation and apoptosis in heart disease.

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • RNA Biology

Background:

  • Long non-coding RNAs (lncRNAs) are implicated in heart diseases like myocardial infarction (MI).
  • Both MALAT1 and PDCD4 are upregulated in MI, but their roles are unclear.
  • Understanding their interaction is crucial for MI pathogenesis.

Purpose of the Study:

  • Investigate the mechanism and function of MALAT1 and PDCD4 in myocardial infarction.
  • Elucidate the regulatory axis involving MALAT1, miR-200a-3p, and PDCD4.
  • Determine the impact of this axis on myocardial cell processes.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) to assess gene expression.
  • Loss-of-function assays (siRNA) to study MALAT1 and PDCD4.
  • MTT assay, flow cytometry, and TUNEL assay for cell viability, cycle, and apoptosis.
  • Mechanism studies including RNA binding analysis and rescue assays.

Main Results:

  • MALAT1 and PDCD4 expression increased in MI models and hypoxic myocardial cells.
  • Knockdown of MALAT1 or PDCD4 improved cell viability, cell cycle progression, and reduced apoptosis.
  • MALAT1 acts as a competing endogenous RNA (ceRNA) by sponging miR-200a-3p to upregulate PDCD4.
  • The MALAT1-miR-200a-3p-PDCD4 axis regulates myocardial cell proliferation and apoptosis.

Conclusions:

  • MALAT1 and PDCD4 are key players in myocardial infarction.
  • The MALAT1-miR-200a-3p-PDCD4 axis is a critical regulator of myocardial cell function in MI.
  • This axis presents a potential therapeutic target for myocardial infarction treatment.
Keywords:
Hypoxia-induced myocardial cellMALAT1Myocardial infarctionPDCD4miR-200a-3p

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