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Sex-specific pathways in early cardiac response to pressure overload in mice

世界最新医学信息文摘 2015年第99期 1-1页

作者： Henning Witt Carola Schubert Juliane Jaekel Daniela Fliegner Adam Penkalla Klaus Tiemann Joerg Stypmann Stefan Roepcke sebastian brokat Shokoufeh Mahmoodzadeh Eva Brozova Mercy M.Davidson Patricia Ruiz Noppinger Christian Grohé Vera Regitz-Zagrosek

Pressure overload(PO) first causes cardiac hypertrophy and then heart failure(HF), which are associated with sex differences in cardiac morphology and function. We aimed to identify genes that may cause HF-related sex differences. We used a transverse aortic constriction(TAC) mouse model leading to hypertrophy without sex differences in cardiac function after 2 weeks, but with sex differences in hypertrophy 6 and 9 weeks after TAC. Cardiac gene expression was analyzed 2 weeks after surgery. Deregulated genes were classified into functional gene ontology(GO) categories and used for pathway analysis. Classical marker genes of hypertrophy were similarly upregulated in both sexes(α-actin, ANP, BNP, CTGF). Thirty-five genes controlling mitochondrial function(PGC-1, cytochrome oxidase, carnitine palmitoyl transferase, acyl-CoA dehydrogenase, pyruvate dehydrogenase kinase) had lower expression in males compared to females after TAC. Genes encoding ribosomal proteins and genes associated with extracellular matrix remodeling exhibited relative higher expression in males(collagen 3, matrix metalloproteinase 2, TIMP2, and TGFβ2, all about twofold) after TAC. We confirmed 87% of the gene expression by real-time polymerase chain reaction. By GO classification, female-specific genes were related to mitochondria and metabolism and males to matrix and biosynthesis. Promoter studies confirmed the upregulation of PGC-1 by E2. Less downregulation of metabolic genes in female hearts and increased protein synthesis capacity and deregulation of matrix remodeling in male hearts characterize the sex-specific early response to PO. These differences could contribute to subsequent sex differences in cardiac function and HF.

关键词： Pressure overload Hypertrophy Gene expression Sex Heart

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Sex-specific pathways in early cardiac response to pressure overload in mice

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世界最新医学信息文摘 2015年第A期 8-8页

Pressure overload(PO) first causes cardiac hypertrophy and then heart failure(HF), which are associated with sex differences in cardiac morphology and function. We aimed to identify genes that may cause HF-related sex differences. We used a transverse aortic constriction(TAC) mouse model leading to hypertrophy without sex differences in cardiac function after 2 weeks, but with sex differences in hypertrophy 6 and 9 weeks after TAC. Cardiac gene expression was analyzed 2 weeks after surgery. Deregulated genes were classified into functional gene ontology(GO) categories and used for pathway analysis. Classical marker genes of hypertrophy were similarly upregulated in both sexes(α-actin, ANP, BNP, CTGF). Thirty-five genes controlling mitochondrial function(PGC-1, cytochrome oxidase, carnitine palmitoyl transferase, acyl-Co A dehydrogenase, pyruvate dehydrogenase kinase) had lower expression in males compared to females after TAC. Genes encoding ribosomal proteins and genes associated with extracellular matrix remodeling exhibited relative higher expression in males(collagen 3, matrix metalloproteinase 2, TIMP2, and TGFβ2, all about twofold) after TAC. We confirmed 87% of the gene expression by real-time polymerase chain reaction. By GO classification, female-specific genes were related to mitochondria and metabolism and males to matrix and biosynthesis. Promoter studies confirmed the upregulation of PGC-1 by E2. Less downregulation of metabolic genes in female hearts and increased protein synthesis capacity and deregulation of matrix remodeling in male hearts characterize the sex-specific early response to PO. These differences could contribute to subsequent sex differences in cardiac function and Hf.

关键词： Pressure overload Hypertrophy Gene expression Sex Heart

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Sex-specific pathways in early cardiac response to pressure overload in mice

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世界最新医学信息文摘 2016年第2期 8-8页

Pressure overload(PO) first causes cardiac hypertrophy and then heart failure(HF),which are associated with sex differences in cardiac morphology and *** aimed to identify genes that may cause HF-related sex *** used a transverse aortic constriction(TAC) mouse model leading to hypertrophy without sex differences in cardiac function after 2 weeks,but with sex differences in hypertrophy 6 and 9 weeks after *** gene expression was analyzed 2 weeks after *** genes were classified into functional gene ontology(GO) categories and used for pathway *** marker genes of hypertrophy were similarly upregulated in both sexes(α-actin,ANP,BNP,CTGF).Thirty-five genes controlling mitochondrial function(PGC-1,cytochrome oxidase,carnitine palmitoyl transferase,acyl-CoA dehydrogenase,pyruvate dehydrogenase kinase) had lower expression in males compared to females after *** encoding ribosomal proteins and genes associated with extracellular matrix remodeling exhibited relative higher expression in males(collagen 3,matrix metalloproteinase 2,TIMP2,and TGFβ2,all about twofold) after *** confirmed 87% of the gene expression by real-time polymerase chain *** GO classification,female-specific genes were related to mitochondria and metabolism and males to matrix and *** studies confirmed the upregulation of PGC-1 by *** downregulation of metabolic genes in female hearts and increased protein synthesis capacity and deregulation of matrix remodeling in male hearts characterize the sex-specific early response to *** differences could contribute to subsequent sex differences in cardiac function and HF.

关键词： Pressure overload Hypertrophy Gene expression Sex Heart

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