ArticleImmunity, inflammation and disease2025
DEL-1 Protects the Myocardium From Ischemia/Hypoxia Injury Through Regulating the Sirt1/NF-κB Signaling Pathway.
Article in Immunity, inflammation and disease, 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
purposeOur study intended to explore the function and the potential mechanisms of developmental endothelial locus-1 (DEL-1) to alleviate myocardial infarction (MI).
methodsFirst, adeno-associated viral containing DEL-1 cDNA was injected into the myocardium of SD rats, and pcDNA-DEL-1 or Sirt1 siRNA was transfected into cardiomyocytes. Next, an MI model in vivo and a hypoxia model in vitro were established. The expression of DEL-1 in MI rats and hypoxia-induced cardiomyocytes was detected by qRT-PCR, Western blot analysis, and immunofluorescence staining. The functions of DEL-1 in vivo were investigated utilizing qRT-PCR, echocardiography, hematoxylin and eosin staining, Masson's trichrome staining, Western blot analysis, TUNEL staining, and detection of hemodynamics, lactate dehydrogenase, and creatine kinase-MB. The functions of DEL-1 in vitro were investigated utilizing qRT-PCR, Western blot analysis, ELISA, flow cytometry, co-culture of cardiac cardiomyocytes and fibroblasts, transwell assay, and immunofluorescence staining.
resultsDEL-1 expression was downregulated in MI rats and hypoxia-induced cardiomyocytes. DEL-1 overexpression alleviated cardiac dysfunction, myocardial fibrosis, inflammation, and cardiomyocyte apoptosis in MI rats. In vitro, DEL-1 overexpression alleviated cardiomyocyte apoptosis and inflammation. Moreover, we also confirmed that DEL-1 secreted by cardiomyocytes activated cardiac fibroblasts through paracrine signaling. Besides, DEL-1 regulated the Sirt1/NF-κB pathway in vitro and in vivo. However, the downregulation of Sirt1 reversed the effect of DEL-1 on cardiomyocyte apoptosis and inflammation.
conclusionDEL-1 could alleviate myocardial damage induced by MI via regulating the Sirt1/NF-κB signaling pathway.
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