microRNA-338-3p suppresses lipopolysaccharide-induced inflammatory response in HK-2 cells
Abstract Background Inflammation is the most common cause of kidney damage, and inflammatory responses in a number of diseases are mediated by microRNA-338-3p (miR-338-3p). However, there are only a few reports which described the regulation of miR-338-3p in human proximal tubular cells. The goal of...
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BMC
2022-12-01
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Series: | BMC Molecular and Cell Biology |
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Online Access: | https://doi.org/10.1186/s12860-022-00455-0 |
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author | Jing Wang Guokai Li Min Lin Sheng Lin Ling Wu |
author_facet | Jing Wang Guokai Li Min Lin Sheng Lin Ling Wu |
author_sort | Jing Wang |
collection | DOAJ |
description | Abstract Background Inflammation is the most common cause of kidney damage, and inflammatory responses in a number of diseases are mediated by microRNA-338-3p (miR-338-3p). However, there are only a few reports which described the regulation of miR-338-3p in human proximal tubular cells. The goal of this study was to see how miR-338-3p affected lipopolysaccharide (LPS)-caused inflammatory response in HK-2 cells. Methods LPS was used to construct an inflammatory model in HK-2 cells. miR-338-3p mimic was used to increase the levels of miR-338-3p in HK-2 cells. MTT, JC-1 staining, and apoptosis assays were used to detect cell viability, mitochondrial membrane potential (MMP), and apoptosis, respectively. The production of inflammatory factors and the levels of p38, p65, phospho-p65, phospho-p38, Bax, Bcl-2, cleaved caspase-9, and cleaved caspase-3 were investigated using real-time polymerase chain reaction, western blotting, or enzyme-linked immunosorbent assay. Results The levels of miR-338-3p were significantly lower in serum from patients with sepsis-induced kidney injury compared to the serum from healthy volunteers (P < 0.05). LPS reduced the level of miR-338-3p in HK-2 cells (P < 0.05). HK-2 cell viability, mitochondrial membrane potential, and Bcl-2 mRNA and protein levels were decreased by LPS (all P < 0.05). Apoptosis, the mRNA and protein levels of inflammatory cytokines (IL-1β, IL-6, IL-8, and TNF-α) and Bax, and the levels of cleaved caspase-9 and caspase-3 were increased by LPS (all P < 0.05). Raising the level of miR-338-3p mitigated these effects of LPS (all P < 0.05). Conclusion LPS-induced inflammation in HK-2 cells is reduced by miR-338-3p. |
first_indexed | 2024-04-11T05:03:44Z |
format | Article |
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institution | Directory Open Access Journal |
issn | 2661-8850 |
language | English |
last_indexed | 2024-04-11T05:03:44Z |
publishDate | 2022-12-01 |
publisher | BMC |
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series | BMC Molecular and Cell Biology |
spelling | doaj.art-feaded6801404071b7702e807d89515e2022-12-25T12:33:51ZengBMCBMC Molecular and Cell Biology2661-88502022-12-0123111010.1186/s12860-022-00455-0microRNA-338-3p suppresses lipopolysaccharide-induced inflammatory response in HK-2 cellsJing Wang0Guokai Li1Min Lin2Sheng Lin3Ling Wu4Department of nosocomial infection management, Fujian Maternity and Child Health HospitalDepartment of nosocomial infection management, Fujian Maternity and Child Health HospitalPediatric intensive care unit, Fujian Maternity and Child Health HospitalDepartment of pediatrics, Fujian Maternity and Child Health HospitalDepartment of pediatrics, Fujian Maternity and Child Health HospitalAbstract Background Inflammation is the most common cause of kidney damage, and inflammatory responses in a number of diseases are mediated by microRNA-338-3p (miR-338-3p). However, there are only a few reports which described the regulation of miR-338-3p in human proximal tubular cells. The goal of this study was to see how miR-338-3p affected lipopolysaccharide (LPS)-caused inflammatory response in HK-2 cells. Methods LPS was used to construct an inflammatory model in HK-2 cells. miR-338-3p mimic was used to increase the levels of miR-338-3p in HK-2 cells. MTT, JC-1 staining, and apoptosis assays were used to detect cell viability, mitochondrial membrane potential (MMP), and apoptosis, respectively. The production of inflammatory factors and the levels of p38, p65, phospho-p65, phospho-p38, Bax, Bcl-2, cleaved caspase-9, and cleaved caspase-3 were investigated using real-time polymerase chain reaction, western blotting, or enzyme-linked immunosorbent assay. Results The levels of miR-338-3p were significantly lower in serum from patients with sepsis-induced kidney injury compared to the serum from healthy volunteers (P < 0.05). LPS reduced the level of miR-338-3p in HK-2 cells (P < 0.05). HK-2 cell viability, mitochondrial membrane potential, and Bcl-2 mRNA and protein levels were decreased by LPS (all P < 0.05). Apoptosis, the mRNA and protein levels of inflammatory cytokines (IL-1β, IL-6, IL-8, and TNF-α) and Bax, and the levels of cleaved caspase-9 and caspase-3 were increased by LPS (all P < 0.05). Raising the level of miR-338-3p mitigated these effects of LPS (all P < 0.05). Conclusion LPS-induced inflammation in HK-2 cells is reduced by miR-338-3p.https://doi.org/10.1186/s12860-022-00455-0MicroRNAInflammationKidney injuryLipopolysaccharideMitochondrial membrane potential |
spellingShingle | Jing Wang Guokai Li Min Lin Sheng Lin Ling Wu microRNA-338-3p suppresses lipopolysaccharide-induced inflammatory response in HK-2 cells BMC Molecular and Cell Biology MicroRNA Inflammation Kidney injury Lipopolysaccharide Mitochondrial membrane potential |
title | microRNA-338-3p suppresses lipopolysaccharide-induced inflammatory response in HK-2 cells |
title_full | microRNA-338-3p suppresses lipopolysaccharide-induced inflammatory response in HK-2 cells |
title_fullStr | microRNA-338-3p suppresses lipopolysaccharide-induced inflammatory response in HK-2 cells |
title_full_unstemmed | microRNA-338-3p suppresses lipopolysaccharide-induced inflammatory response in HK-2 cells |
title_short | microRNA-338-3p suppresses lipopolysaccharide-induced inflammatory response in HK-2 cells |
title_sort | microrna 338 3p suppresses lipopolysaccharide induced inflammatory response in hk 2 cells |
topic | MicroRNA Inflammation Kidney injury Lipopolysaccharide Mitochondrial membrane potential |
url | https://doi.org/10.1186/s12860-022-00455-0 |
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