ArticleCytotechnology2025
miR-361-5p regulates acute infective endocarditis by mediating SLPI/NF-κB signaling pathway.
Article in Cytotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Acute infective endocarditis (AIE) is an inflammatory reaction caused by the infection of the endocardial surface, accompanied by the formation of vegetation with different shapes and sizes. miR-361-5p and secretory leukocyte protease inhibitor (SLPI) were reported to mediate the process of staphylococcus aureus (SA) infection in AIE, but their roles in AIE are unclear. In this study, the AIE cell model was induced by hypoxia and infection of SA, and the AIE rat model was established. Dual-luciferase experiment was performed to verify the interaction between miR-361-5p and SLPI. Reverse transcription real-time polymerase chain reaction (RT-qPCR), western blot, Cell counting kit-8, flow cytometry, and Enzyme-linked immunosorbent assay (ELISA) kits were used to detect the role of miR-361-5p and SLPI in AIE cells. Hematoxylin and eosin staining, RT-qPCR, western blot, Terminal deoxynucleotidyl transferase dUTP nick end-labeling staining and ELISA kits were used to detect the function of miR-361-5p and SLPI in AIE rats. Mechanistic research revealed that miR-361-5p targeted SLPI. miR-361-5p was highly expressed in AC16 cells induced by hypoxia and SA, while SLPI expression was decreased. Compared with the NC group, hypoxia and SA infection-induced AIE model cells exhibited significantly reduced cell viability, elevated apoptosis rates, increased concentrations of creatine kinase-MB (CK-MB), cardiac troponin T (cTnT), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α), as well as activation of nuclear factor-kappa B p65 (NF-κB p65). Knockdown of miR-361-5p or overexpression of SLPI increased AC16 cell viability, reduced AIE-induced apoptosis rates, decreased CK-MB, cTnT, IL-1β, and TNF-α levels, and suppressed NF-κB p65 activation. Knockdown of SLPI reversed the effects of miR-361-5p knockdown on AC16 cells. In vivo results demonstrated that knockdown of miR-361-5p suppressed valvular vegetation formation in rats with AIE, reduced myocardial apoptosis, and decreased levels of CK-MB, cTnT, IL-1β, and TNF-α. Our study demonstrates that knockdown of miR-361-5p has a protective effect on AIE by promoting SLPI and inhibiting NF-κB P65 signalling pathway, which may provide a new perspective for treating AIE.
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