Long noncoding RNA MALAT1 can regulate proliferation and apoptosis of LPS-treated HK-2 cells via targeting miR-23a-3p through regulating ERK signaling
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 heal...
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| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
| Published: |
Termedia Publishing House
2020-04-01
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| Series: | Archives of Medical Science |
| Subjects: | |
| Online Access: | https://www.archivesofmedicalscience.com/Long-noncoding-RNA-MALAT1-can-regulate-proliferation-and-apoptosis-of-LPS-treated,119783,0,2.html |
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| Summary: | 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. |
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| ISSN: | 1734-1922 1896-9151 |