Inactivation of 14-3-3 Protein Exacerbates Cardiac Hypertrophy and Fibrosis through Enhanced Expression of Protein Kinase C β2 in Experimental Diabetes(Biochemistry/Molecular Biology)

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概要

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• Diabetic cardiomyopathy is associated with cardiac hypertrophy and fibrosis. Activation of protein kinase C (PKC) has been implicated in the diabetes-induced cardiovascular complications. PKCβ2 isoform is preferentially found to be activated in the diabetic myocardium. However, the role of PKCβ2 in diabetic cardiomyopathy is not clear. 14-3-3 family members are dimeric phosphoserine-binding proteins that regulate signal transduction, apoptotic and checkpoint control pathways, and have been shown to bind with PKC isozymes and negatively regulate their enzymatic activities. The present study tests whether 14-3-3 protein regulates cardiac hypertrophy and fibrosis in streptozotocin (STZ)-induced diabetic mice, using transgenic mice with cardiac specific over-expression of dominant negative (DN) 14-3-3 protein. In addition, we examined the relationship between 14-3-3 protein and PKCβ2 in the diabetic myocardium. Cardiac myocyte diameter, content of cardiac fibrosis, left ventricular tissue expressions of atrial natriuretic peptide, transforming growth factor β1, collagen III and PKCβ2 were significantly elevated 28 and 56d after STZ injection in transgenic DN-14-3-3 mice, when compared to their non-transgenic counterparts. These results clearly demonstrate that the functional inactivation of 14-3-3 protein in DN-14-3-3 mice exacerbates diabetes-induced cardiac hypertrophy and fibrosis. The exacerbations of cardiac hypertrophy and fibrosis were significantly and positively correlated with the enhanced expression of PKCβ2 in DN-14-3-3 mice. Our results indicate for the first time that 14-3-3 protein negatively regulates cardiac hypertrophy and fibrosis, possibly through controlling the expression of PKCβ2 in the diabetic myocardium.

• 公益社団法人日本薬学会の論文
• 2005-06-01

著者

• Watanabe Kenichi

  Department of Clinical Pharmacology, Niigata University of Pharmacy and Applied Life Sciences

• Watanabe Kenichi

  新潟大学 医歯学総合研究科循環器学

• Aizawa Yoshifusa

  First Department of Internal Medicine, Niigata University School of Medicine

• Aizawa Y

  Division Of Cardiology Niigata University Graduate School Of Medical And Dental Sciences

• Kodama Makoto

  First Department of Internal Medicine, Division of Cardiology, Niigata University School of Medicine

• GURUSAMY Narasimman

  Department of Anesthesiology and Medicine, Brigham and Women's Hospital, Harvard Medical School

• MA Meilei

  Department of Clinical Pharmacology, Faculty of Pharmaceutical Sciences, Niigata University of Pharm

• Ma Meilei

  Department Of Clinical Pharmacology Faculty Of Pharmaceutical Sciences Niigata University Of Pharmac

• Watanabe Kenichi

  Department Of Clinical Pharmacology Faculty Of Pharmaceutical Sciences Niigata University Of Pharmac

• Zhang Shaosong

  米国

• Gurusamy Narasimman

  Department Of Anesthesiology And Medicine Brigham And Women's Hospital Harvard Medical School

• ZHANG Shaosong

  Departments of Cell Biology and Physiology, Center for Cardiovascular Research, Washington Universit

• MUSLIN Anthony

  Departments of Cell Biology and Physiology, Center for Cardiovascular Research, Washington Universit

• Muslin Anthony

  Departments Of Cell Biology And Physiology Center For Cardiovascular Research Washington University

• Zhang Shaosong

  Departments Of Cell Biology And Physiology Center For Cardiovascular Research Washington University

• Aizawa Y

  新潟大学 内科

• Watanabe K

  Cardiovascular Division Tsubame Rosai Hospital

• Watanabe Kenichi

  Division Of Cardiology Tsubame Rosai Hospital

• Aizawa Yoshifusa

  First Department Of Internal Medicine Niigata Universaity School Of Medicine

• Kodama Makoto

  First Dep. Of Medicine Graduate School Of Medical And Dental Sciences Niigata Univ.

• Watanabe Kenichi

  燕労災病院

• AIZAWA Yoshifusa

  First Department of Internal Medecine, Niigata University School of Medicine, Niigata, Japan.

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