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Published on: November 3, 2014
microRNA-338-3p suppresses lipopolysaccharide-induced inflammatory response in HK-2 cells
Jing Wang1, Guokai Li1, Min Lin2
1Department of nosocomial infection management, Fujian Maternity and Child Health Hospital, Fujian, Fuzhou, 350001, China.
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.
Insights
MicroRNA-338-3p (miR-338-3p) plays a protective role in kidney injury. Increasing miR-338-3p levels can mitigate lipopolysaccharide (LPS)-induced inflammation in human proximal tubular HK-2 cells.
Area of Science:
- Nephrology
- Molecular Biology
- Immunology
Background:
- Inflammation is a primary driver of kidney damage.
- MicroRNA-338-3p (miR-338-3p) is implicated in inflammatory responses across various diseases.
- Limited research exists on miR-338-3p regulation in human proximal tubular cells.
Purpose of the Study:
- To investigate the role of miR-338-3p in lipopolysaccharide (LPS)-induced inflammation in HK-2 cells.
- To determine if modulating miR-338-3p levels impacts inflammatory pathways in kidney cells.
Main Methods:
- An LPS-induced inflammation model was established in HK-2 cells.
- miR-338-3p levels were manipulated using mimics.
- Cell viability, mitochondrial membrane potential, and apoptosis were assessed.
- Inflammatory factor production and key protein/gene expression (p38, p65, Bax, Bcl-2, caspases) were quantified.
Main Results:
- LPS significantly reduced miR-338-3p levels in HK-2 cells.
- LPS decreased cell viability, mitochondrial membrane potential, and Bcl-2 expression.
- LPS increased apoptosis, inflammatory cytokine production (IL-1β, IL-6, IL-8, TNF-α), and Bax, cleaved caspase-9, and cleaved caspase-3 levels.
- Upregulating miR-338-3p counteracted the detrimental effects of LPS.
Conclusions:
- miR-338-3p exhibits a protective effect against LPS-induced inflammation in HK-2 cells.
- Restoring miR-338-3p levels can ameliorate LPS-induced kidney cell damage and inflammation.
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