To investigate whether Bmi-l deficiency lead to intestinal epithelial barrier destruction and microbiota dysfunction and whether p16 deletion could reverse the damage of intestinal epithelial barrier and microbial dys...To investigate whether Bmi-l deficiency lead to intestinal epithelial barrier destruction and microbiota dysfunction and whether p16 deletion could reverse the damage of intestinal epithelial barrier and microbial dysbiosis.Bmi-l and pl6 double-knockout(Bmi-17 pl6/)mice were generated.The barrier structure and function of epithelium,the species,abundance,and function of microflora,and proinflammation of macrophages in intestine were compared with Bmi-l/and wild-type(WT)mice.Bone marrow derived macrophages were infected with fecal mixed bacteria for observing proinflammation.展开更多
To study whether Bmi-l maintained cardiac function and prevents senescence associated pathological cardiac hypertrophy(PCH)and whether Bmi-1-RING1B promoted GATA4 ubiquitination and its autophagic degradation for prev...To study whether Bmi-l maintained cardiac function and prevents senescence associated pathological cardiac hypertrophy(PCH)and whether Bmi-1-RING1B promoted GATA4 ubiquitination and its autophagic degradation for preventing senescence-related PCH,Bmi^(-/-)deficient(Bmi^(-/-))mice and WT littermates were directly observed for PCH;Bmi-1+,Bmi^(-/-)overexpression transgenic(Bmi1^(TM))and WT mice were indirectly subcutaneously infused AngⅡto recur the development of PCH and observed;A utophagy agonist metformin or rapamycin was administered to Bmi^(-/-)and WT mice infused with AngⅡ.Mouse embryonic cardiomyocyte(ECM)and human myocardial AC16 cells were used for experiments.Phenotypes of cardiac and cardiomyocytes and GATA4-autophagic degradation were analyzed.展开更多
文摘To investigate whether Bmi-l deficiency lead to intestinal epithelial barrier destruction and microbiota dysfunction and whether p16 deletion could reverse the damage of intestinal epithelial barrier and microbial dysbiosis.Bmi-l and pl6 double-knockout(Bmi-17 pl6/)mice were generated.The barrier structure and function of epithelium,the species,abundance,and function of microflora,and proinflammation of macrophages in intestine were compared with Bmi-l/and wild-type(WT)mice.Bone marrow derived macrophages were infected with fecal mixed bacteria for observing proinflammation.
文摘To study whether Bmi-l maintained cardiac function and prevents senescence associated pathological cardiac hypertrophy(PCH)and whether Bmi-1-RING1B promoted GATA4 ubiquitination and its autophagic degradation for preventing senescence-related PCH,Bmi^(-/-)deficient(Bmi^(-/-))mice and WT littermates were directly observed for PCH;Bmi-1+,Bmi^(-/-)overexpression transgenic(Bmi1^(TM))and WT mice were indirectly subcutaneously infused AngⅡto recur the development of PCH and observed;A utophagy agonist metformin or rapamycin was administered to Bmi^(-/-)and WT mice infused with AngⅡ.Mouse embryonic cardiomyocyte(ECM)and human myocardial AC16 cells were used for experiments.Phenotypes of cardiac and cardiomyocytes and GATA4-autophagic degradation were analyzed.
