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MicroRNA-214-3p Ameliorates LPS-Induced Cardiomyocyte Injury by Inhibiting Cathepsin B
1The First Affiliated Hospital, Department of Cardiovascular Surgery, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China.
Abstract:
Myocardial injury is a common complication of sepsis. MicroRNA (miRNA) miR-214-3p is protective against myocardial injury caused by sepsis, but its mechanism in lipopolysaccharide (LPS)- induced cardiomyocyte injury is still unclear. An AC16 cell injury model was induced by LPS treatment. Cell Counting Kit-8 and flow cytometry assay showed decreased cell viability and increased apoptosis in LPS-treated AC16 cells. The levels of caspase- 3, Bax, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), myosin 6 (Myh6), myosin 7 (Myh7), reactive oxygen species (ROS), and malondialdehyde (MDA) were increased in LPS-treated AC16 cells, but the levels of Bcl-2 and superoxide dismutase (SOD) were decreased. MiR-214-3p was down-regulated and cathepsin B (CTSB) was upregulated in LPS-treated AC16 cells. At the same time, miR-214-3p could target CTSB and reduce its expression. We also found that a miR-214-3p mimic or CTSB silencing could significantly reduce LPSinduced apoptosis, decrease ROS, MDA, caspase-3, and Bax and increase SOD and Bcl-2. CTSB silencing could significantly reduce ANP, BNP, Myh6, and Myh7 in LPS-treated AC16 cells. The effects of CTSB silencing were reversed by a miR-214-3p inhibitor. In summary, miR-214-3p could inhibit LPSinduced myocardial injury by targeting CTSB, which provides a new idea for myocardial damage caused by sepsis.
Insights
MicroRNA miR-214-3p protects against sepsis-induced myocardial injury by targeting cathepsin B (CTSB). This study reveals miR-214-3p inhibits cardiomyocyte damage, offering new therapeutic strategies for sepsis complications.
Area of Science:
- Cardiology
- Molecular Biology
- Cell Biology
Background:
- Myocardial injury is a frequent sepsis complication.
- The protective role of microRNA (miRNA) miR-214-3p in sepsis-induced myocardial injury is established, but its precise mechanism remains unclear.
- Lipopolysaccharide (LPS) is a key component in inducing sepsis-related cellular damage.
Purpose of the Study:
- To elucidate the mechanism by which miR-214-3p exerts its protective effects against LPS-induced cardiomyocyte injury.
- To investigate the potential interaction between miR-214-3p and cathepsin B (CTSB) in the context of myocardial injury.
Main Methods:
- AC16 cells were treated with LPS to establish a cardiomyocyte injury model.
- Cell viability, apoptosis, and levels of key proteins (caspase-3, Bax, Bcl-2, ANP, BNP, Myh6, Myh7) and oxidative stress markers (ROS, MDA, SOD) were assessed.
- Expression levels of miR-214-3p and CTSB were analyzed, and their regulatory relationship was investigated using miR-214-3p mimics, inhibitors, and CTSB silencing.
Main Results:
- LPS treatment decreased AC16 cell viability and increased apoptosis, alongside elevated caspase-3, Bax, ROS, MDA, ANP, BNP, Myh6, and Myh7, while decreasing Bcl-2 and SOD.
- miR-214-3p was downregulated, and CTSB was upregulated in LPS-treated cells, with miR-214-3p directly targeting and reducing CTSB expression.
- Overexpression of miR-214-3p or silencing of CTSB significantly attenuated LPS-induced apoptosis and oxidative stress, restoring cellular protective mechanisms. CTSB silencing also reduced cardiac marker expression, effects reversed by miR-214-3p inhibition.
Conclusions:
- miR-214-3p plays a critical protective role in mitigating LPS-induced myocardial injury by targeting and downregulating CTSB.
- This molecular pathway involving miR-214-3p and CTSB offers a novel therapeutic target for managing sepsis-associated myocardial damage.
