Key result
Silencing TNNI3K reduces myocardial injury and apoptosis in H9C2 cells by regulating apoptosis-related proteins.
Why the study?
The study was conducted to investigate the effect of cardiac troponin I-interacting kinase on sepsis-induced myocardial dysfunction and explore the underlying molecular mechanisms.
Does silencing TNNI3K reduce LPS-induced myocardial injury and apoptosis in H9C2 cells?
Does silencing TNNI3K reduce LPS-induced myocardial injury and apoptosis in H9C2 cells?
Silencing TNNI3K alleviates LPS-induced myocardial injury in vitro by regulating apoptosis-related proteins, suggesting a potential therapeutic target for sepsis-induced myocardial dysfunction.
TNNI3K silencing may protect against inflammatory cardiomyocyte injury; leaves open translation to in vivo models or clinical sepsis.
The aim of this study was to investigate the effect of cardiac troponin I‐interacting kinase (TNNI3K) on sepsis‐induced myocardial dysfunction (SIMD) and further explore the underlying molecular mechanisms. In this study, a lipopolysaccharide‐ (LPS‐) induced myocardial injury model was used. qRT‐PCR was performed to detect the mRNA expression of TNNI3K. Western blot was conducted to quantitatively detect the expression of TNNI3K and apoptosis‐related proteins (Bcl‐2, Bax, and caspase‐3). ELISA was performed to detect the content of lactate dehydrogenase (LDH) and creatine kinase (CK). TUNEL assay was used to detect the apoptosis of H9C2 cells. In LPS‐induced H9C2 cells, TNNI3K was up regulated. Besides, the CK activity, the content of LDH, and the apoptosis of H9C2 cells were significantly increased after treatment with LPS. Silencing TNNI3K decreased the LDH release activity and CK activity and inhibited apoptosis of H9C2 cell. Further research illustrated that si‐TNNI3K promoted the protein expression of Bcl‐2 and decreased the protein expression of Bax and cleaved caspase‐3. The study concluded that TNNI3K was upregulated in LPS‐induced H9C2 cells. Importantly, functional research findings indicated that silencing TNNI3K alleviated LPS‐induced H9C2 cell injury by regulating apoptosis‐related proteins.
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Dong et al. (2021) studied Sepsis-induced myocardial dysfunction. Silencing TNNI3K vs. LPS treatment alone was evaluated on Myocardial injury (LDH, CK) and apoptosis. Silencing TNNI3K decreased LDH release, CK activity, and apoptosis in lipopolysaccharide-induced H9C2 cells by regulating apoptosis-related proteins.
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