Long noncoding RNA MALAT1 can regulate proliferation and apoptosis of LPS-treated HK-2 cells via targeting miR-23a-3p

Jinxia Li1, Haibo Liu2, Chao Li2

  • 1Department of Critical Care, Dongfang Hospital, Beijing University of Chinese Medicine, Beijing, China.

Abstract

Insights

Long noncoding RNA MALAT1 is elevated in sepsis-induced acute kidney injury. MALAT1 regulates cell proliferation and apoptosis via the miR-23a-3p and ERK signaling pathway, offering a potential therapeutic target.

Area of Science:

  • Molecular Biology
  • Renal Physiology

Background:

  • Sepsis-induced acute kidney injury (septic AKI) is a critical condition with high mortality.
  • Long noncoding RNAs (lncRNAs) are increasingly recognized for their roles in various diseases, including AKI.

Purpose of the Study:

  • To investigate the role of lncRNA MALAT1 in septic AKI.
  • To elucidate the underlying molecular mechanism involving miR-23a-3p and ERK signaling.

Main Methods:

  • Serum samples from septic AKI patients and healthy controls were analyzed for MALAT1 levels.
  • In vitro experiments using LPS-treated HK-2 cells assessed the effects of MALAT1 and miR-23a-3p on cell proliferation and apoptosis.
  • The involvement of ERK signaling was investigated.

Main Results:

  • MALAT1 levels were significantly increased in septic AKI patients and LPS-treated cells.
  • Overexpression of MALAT1 mitigated LPS-induced kidney cell injury.
  • MALAT1 was confirmed to target miR-23a-3p, and MALAT1 siRNA promoted cell proliferation and inhibited apoptosis by activating ERK signaling.
  • Knockdown of miR-23a-3p partially reversed the anti-apoptotic effects of MALAT1 siRNA.

Conclusions:

  • The MALAT1/miR-23a-3p axis plays a crucial role in regulating proliferation and apoptosis in septic AKI.
  • This axis modulates ERK signaling, suggesting it as a potential therapeutic target for septic AKI.

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