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miR-128-3p inhibits apoptosis and inflammation in LPS-induced sepsis by targeting TGFBR2
Peng Yang1, Jianhua Han2, Shigeng Li2
1Department of Anesthesiology, The First Affiliated Hospital, Sun Yat-sen University, 510080, Guangzhou, China.
Background:
Sepsis is a systemic inflammatory response that can lead to the dysfunction of many organs. The aberrant expression of miRNAs is associated with the pathogenesis of sepsis. However, the biological functions of miR-128-3p in sepsis remain largely unknown, and its mechanism should be further investigated. This study aimed to determine the regulatory network of miR-128-3p and TGFBR2 in lipopolysaccharide (LPS)-induced sepsis.
Methods:
The expression levels of miR-128-3p and transforming growth factor beta receptors II (TGFBR2) were detected by quantitative polymerase chain reaction (qPCR). The protein levels of TGFBR2, Bcl-2, Bax, cleaved caspase 3, Smad2, and Smad3 were measured by western blot. Cell apoptosis was analyzed by flow cytometry. Cytokine production was detected by enzyme-linked immunosorbent assay (ELISA). The binding sites of miR-128-3p and TGFBR2 were predicted by Targetscan online software and confirmed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay.
Results:
The level of miR-128-3p was decreased, and TGFBR2 expression was increased in serum samples of sepsis patients and LPS-induced HK2 cells. Overexpression of miR-128-3p or knockdown of TGFBR2 ameliorated LPS-induced inflammation and apoptosis. Moreover, TGFBR2 was a direct target of miR-128-3p, and its overexpression reversed the inhibitory effects of miR-128-3p overexpression on inflammation and apoptosis in LPS-induced HK2 cells. Besides, overexpression of miR-128-3p downregulated TGFBR2 to suppress the activation of the Smad signaling pathway.
Conclusion:
miR-128-3p could inhibit apoptosis and inflammation by targeting TGFBR2 in LPS-induced HK2 cells, which might provide therapeutic strategy for the treatment of sepsis.
Insights
MicroRNA-128-3p (miR-128-3p) levels decrease in sepsis, leading to increased TGFBR2. Restoring miR-128-3p inhibits inflammation and apoptosis by targeting TGFBR2, offering a potential sepsis treatment.
Area of Science:
- Molecular Biology
- Immunology
- Cell Biology
Background:
- Sepsis involves systemic inflammation and organ dysfunction.
- MicroRNAs (miRNAs) are implicated in sepsis pathogenesis.
- The role of miR-128-3p in sepsis is not well understood.
Purpose of the Study:
- To investigate the regulatory network of miR-128-3p and TGFBR2 in sepsis.
- To elucidate the mechanism of miR-128-3p in lipopolysaccharide (LPS)-induced sepsis.
Main Methods:
- Quantitative PCR and Western blot to measure gene and protein expression.
- Flow cytometry for cell apoptosis analysis.
- ELISA for cytokine detection.
- Dual-luciferase reporter and RIP assays to confirm miRNA-target interaction.
Main Results:
- miR-128-3p was downregulated, and TGFBR2 was upregulated in sepsis patients and LPS-induced cells.
- miR-128-3p overexpression or TGFBR2 knockdown reduced inflammation and apoptosis.
- TGFBR2 is a direct target of miR-128-3p, mediating its effects on inflammation and apoptosis.
- miR-128-3p suppressed the Smad signaling pathway by downregulating TGFBR2.
Conclusions:
- miR-128-3p inhibits apoptosis and inflammation in LPS-induced sepsis by targeting TGFBR2.
- This interaction presents a potential therapeutic strategy for sepsis treatment.
