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Keywords {🔍}

rats, article, pubmed, diabetic, wistar, google, scholar, protein, apoptosis, cardiac, myocardial, cardiomyocyte, increase, cas, heart, increased, expression, figure, hypertrophy, sirt, area, rat, foxoa, akt, study, remodeling, diabetes, phosphorylation, tissue, left, postinfarct, showed, gotokakizaki, infarct, shows, infarction, fibrosis, shamoperated, remote, kinase, weeks, results, size, ventricular, factor, nondiabetic, western, mapk, cell, shown,

Topics {✒️}

atrial natriuretic peptide chico/pi3-kinase signaling pathway short axis view rabbit anti-digoxigenin-ap-conjugate sham-operated goto-kakizaki rats spontaneously diabetic goto-kakizaki open access article diabetic goto-kakizaki rat ville kytö goto-kakizaki rat heart digoxigenin-conjugated dideoxy-utp diabetic goto-kakizaki rats article download pdf post-infarct cardiac remodeling representative m-mode echocardiography sirt1-positive cardiomyocytes/total number shows picrosirius--red stained cardiac p38-mapk pathway mi-induced cardiomyocyte hypertrophy diabetes-induced cardiac hypertrophy author information authors post-infarct gk rats m-mode lv dimensions mi-induced cardiac remodeling improves cardiac function trichrome-stained histological sections akt-mediated phosphorylation foxo3a post-infarct wistar rats accelerate cardiomyocyte growth diabetic goto-kakizaki basic biochemical parameters angiotensin ii-induced inflammation formalin-fixed myocardial sections digoxigenin antibody conjugated lv end-diastolic volume lv end-systolic volume post--mi gk rats post-mi gk rats increased nuclear foxo3a-translocation goto-kakizaki rats sirt1-target protein p53 foxo3a transcription factor digoxigenin-tagged foxo3a oligonucleotides long-term activation anti-phospho-fkhrl/foxo3a foxo3a-regulated target genes methods myocardial infarction post-mi wistar rats forkhead transcription factor increased cardiomyocyte hypertrophy

Questions {❓}

• O'Neill BT, Abel ED: Akt1 in the cardiovascular system: friend of foe?

Schema {🗺️}

WebPage:
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         headline:Sirtuin1-p53, forkhead box O3a, p38 and post-infarct cardiac remodeling in the spontaneously diabetic Goto-Kakizaki rat
         description:Diabetes is associated with changes in myocardial stress-response pathways and is recognized as an independent risk factor for cardiac remodeling. Using spontaneously diabetic Goto Kakizaki rats as a model of type 2 DM we investigated whether post-translational modifications in the Akt - FOXO3a pathway, Sirt1 - p53 pathway and the mitogen activated protein kinase p38 regulator are involved in post-infarct cardiac remodeling Experimental myocardial infarction (MI) was induced by left anterior descending coronary artery ligation in spontaneously diabetic Goto-Kakizaki rats and non-diabetic Wistar controls. Cardiac function was studied by echocardiography. Myocardial hypertrophy, cardiomyocyte apoptosis and cardiac fibrosis were determined histologically 12 weeks post MI or Sham operation. Western blotting was used to study Caspase-3, Bax, Sirt1, acetylation of p53 and phosphorylation of p38, Akt and FOXO3a. Electrophoretic mobility shift assay was used to assess FOXO3a activity and its nuclear localization. Post-infarct heart failure in diabetic GK rats was associated with pronounced cardiomyocyte hypertrophy, increased interstitial fibrosis and sustained cardiomyocyte apoptosis as compared with their non-diabetic Wistar controls. In the GK rat myocardium, Akt- and FOXO3a-phosphorylation was decreased and nuclear localization of FOXO3a was increased concomitantly with increased PTEN protein expression. Furthermore, increased Sirt1 protein expression was associated with decreased p53 acetylation, and phosphorylation of p38 was increased in diabetic rats with MI. Post-infarct heart failure in diabetic GK rats was associated with more pronounced cardiac hypertrophy, interstitial fibrosis and sustained cardiomyocyte apoptosis as compared to their non-diabetic controls. The present study suggests important roles for Akt-FOXO3a, Sirt1 - p53 and p38 MAPK in the regulation of post-infarct cardiac remodeling in type 2 diabetes.
         datePublished:2010-01-27T00:00:00Z
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            Atrial Natriuretic Peptide
            Connective Tissue Growth Factor
            Electrophoretic Mobility Shift Assay
            Cardiomyocyte Apoptosis
            Cardiomyocyte Hypertrophy
            Diabetes
            Angiology
            Cardiology
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      headline:Sirtuin1-p53, forkhead box O3a, p38 and post-infarct cardiac remodeling in the spontaneously diabetic Goto-Kakizaki rat
      description:Diabetes is associated with changes in myocardial stress-response pathways and is recognized as an independent risk factor for cardiac remodeling. Using spontaneously diabetic Goto Kakizaki rats as a model of type 2 DM we investigated whether post-translational modifications in the Akt - FOXO3a pathway, Sirt1 - p53 pathway and the mitogen activated protein kinase p38 regulator are involved in post-infarct cardiac remodeling Experimental myocardial infarction (MI) was induced by left anterior descending coronary artery ligation in spontaneously diabetic Goto-Kakizaki rats and non-diabetic Wistar controls. Cardiac function was studied by echocardiography. Myocardial hypertrophy, cardiomyocyte apoptosis and cardiac fibrosis were determined histologically 12 weeks post MI or Sham operation. Western blotting was used to study Caspase-3, Bax, Sirt1, acetylation of p53 and phosphorylation of p38, Akt and FOXO3a. Electrophoretic mobility shift assay was used to assess FOXO3a activity and its nuclear localization. Post-infarct heart failure in diabetic GK rats was associated with pronounced cardiomyocyte hypertrophy, increased interstitial fibrosis and sustained cardiomyocyte apoptosis as compared with their non-diabetic Wistar controls. In the GK rat myocardium, Akt- and FOXO3a-phosphorylation was decreased and nuclear localization of FOXO3a was increased concomitantly with increased PTEN protein expression. Furthermore, increased Sirt1 protein expression was associated with decreased p53 acetylation, and phosphorylation of p38 was increased in diabetic rats with MI. Post-infarct heart failure in diabetic GK rats was associated with more pronounced cardiac hypertrophy, interstitial fibrosis and sustained cardiomyocyte apoptosis as compared to their non-diabetic controls. The present study suggests important roles for Akt-FOXO3a, Sirt1 - p53 and p38 MAPK in the regulation of post-infarct cardiac remodeling in type 2 diabetes.
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         Atrial Natriuretic Peptide
         Connective Tissue Growth Factor
         Electrophoretic Mobility Shift Assay
         Cardiomyocyte Apoptosis
         Cardiomyocyte Hypertrophy
         Diabetes
         Angiology
         Cardiology
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      name:Institute of Biomedicine, Pharmacology, University of Helsinki, Finland

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