Immunity, inflammation and disease · 2025
DEL-1 Protects the Myocardium From Ischemia/Hypoxia Injury Through Regulating the Sirt1/NF-κB Signaling Pathway.
СтатьяНазвание и аннотация: Перевод в очереди
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Hu Bin, Zhang Wenlong, Yu Wan-Cheng, Lin Hao
Аннотация
PURPOSE: Our study intended to explore the function and the potential mechanisms of developmental endothelial locus-1 (DEL-1) to alleviate myocardial infarction (MI).
METHODS: First, 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.
RESULTS: DEL-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.
CONCLUSION: DEL-1 could alleviate myocardial damage induced by MI via regulating the Sirt1/NF-κB signaling pathway.
METHODS: First, 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.
RESULTS: DEL-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.
CONCLUSION: DEL-1 could alleviate myocardial damage induced by MI via regulating the Sirt1/NF-κB signaling pathway.