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Updated: May 23, 2025

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity
Published on: January 7, 2019
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.
Introduction:
The aim of the present study was to investigate the roles of long noncoding RNA (lncRNA) MALAT1 in the development of sepsis-induced acute kidney injury (septic AKI) and the underlying mechanism.
Material And Methods:
The levels of MALAT1 in the serum of the septic AKI patients and healthy subjects were compared, and the targeting relationship between MALAT1 and miR-23a-3p was analyzed. Moreover, the effects of MALAT1 and miR-23a-3p on the proliferation and apoptosis of LPS-treated HK-2 cells were analyzed. Finally, the roles of ERK signaling during this process were analyzed.
Results:
We found that MALAT1 was markedly increased in serum of the septic AKI patients and LPS-treated cells. In addition, overexpression of MALAT1 relieved the injury induced by LPS in RMCs. Moreover, miR-23-a-3p has been confirmed as a target of MALAT1. Meanwhile, we also found that MALAT1 siRNA can increase the proliferation and inhibit the apoptosis of LPS-treated HK-2 cells through activating ERK signaling, and knockdown of miR-23a-3p can partially block the anti-apoptotic effect of MALAT1 siRNA.
Conclusions:
We report that MALAT1 can regulate the proliferation and apoptosis of LPS-treated HK-2 cells via targeting miR-23a-3p through regulating ERK signaling, suggesting that the MALAT1/miR-23a-3p axis could serve as a potential therapeutic target for the treatment of septic AKI.
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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