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Chinese Journal of Endocrinology and Metabolism ; (12): 48-54, 2023.
Artigo em Chinês | WPRIM | ID: wpr-994296

RESUMO

Objective:To investigate the effect of autophagy related gene Atg101 on white adipocyte senescence.Methods:An Atg101 knockdown model of 3T3-L1 mature adipocytes was constructed to probe the effect of Atg101 on autophagy-related proteins LC3 and p62 protein. The RNA-seq database of human subcutaneous adipose tissue was constructed and analyzed, and the co-expressed gene set was predicted based on the pearson correlation coefficient( R2>0.4, P<0.05) between FPKM values of Atg101 and other gene, followed by KEGG and Reactome enrichment analysis. Young mouse(8 weeks old) and old mouse(18 months old) models were established, and the expression levels of Atg101 in inguinal white adipose tissue and epididymal white adipose tissue were detected by quantitative real-time PCR(RT-qPCR) and Western blot. Furthermore, the differences in white adipocyte senescence-associated secretory phenotype(SASP), cell cycle and mitochondrial homeostasis-related genes were detected by RNA-seq, Western blot, and RT-qPCR to analyze the effects of Atg101 silencing on adipocyte senescence. Results:The autophagy-related protein LC3-Ⅱ expression was significantly decreased and p62 protein was induced after Atg101 was knockdowned in 3T3-L1 adipocytes, suggesting impaired cell autophagy. KEGG enrichment analysis revealed that Atg101 co-expressed gene set was mainly enriched in autophagy and senescence-related pathways; Reactome enrichment analysis revealed that this gene set was associated with multiple cell cycle signaling pathways. RT-qPCR and Western blot confirmed that both mRNA and protein levels of Atg101 were down-regulated in inguinal white adipose tissue of aging mice, and protein levels in epididymal white adipose tissue were also significantly reduced. Finally, it was further confirmed that SASP-related genes were induced after Atg101 knockdown in white adipocytes, and cell cycle-specific gene expression was restricted and cytokine-dependent protein kinase inhibitors p16 and p21 expressions were significantly increased, while mitochondrial homeostasis regulatory genes were also suppressed.Conclusions:Knockdown of Atg101 may regulate white adipocyte senescence by inhibiting autophagic activity, presenting impaired mitochondrial homeostasis.

2.
Chinese Journal of Primary Medicine and Pharmacy ; (12): 2635-2636, 2011.
Artigo em Chinês | WPRIM | ID: wpr-422010

RESUMO

ObjectiveTo explore the value of color Doppler echocardiography in diagnosing apical hypertrophic cardiomyopathy( apical hypertrophic cardiomyopathy, AHCM). MethodsRetrospective analysis of 28 cases with apical hypertrophic cardiomyopathy by echocardiography images was carried out. Results28 cases AHCM patients,apical myocardial thickness 17 ~29mm,5 cases of simple apical myocardial thickening;10 cases of ventricular apex、left ventricular myocardial wall thickening in the apical segment;6 cases of ventricular apex、left ventricular myocardial thickening of apical segments of inferior;6 cases of Ventricular apex,left ventricular free wall thickening of apical myocardial; 1 case of ventricular apex、right ventricular free wall thickening of apical myocardial. All patients were diagnosed. ConclusionColor Doppler echocardiograph was an effective method for diagnosis of apical hypertrophic cardiomyopathy.

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