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Deletion of Akt1 causes heart defects and abnormal cardiomyocyte proliferation.pdf

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Deletion of Akt1 causes heart defects and abnormal cardiomyocyte proliferation

Developmental Biology 347 (2010) 384–391 Contents lists available at ScienceDirect Developmental Biology j ourna l homepage: www.e lsev ie /deve lopmenta lb io logyGenomes Developmental Control Deletion of Akt1 causes heart defects and abnormal cardiomyocyte proliferation Zai Chang a, Qin Zhang a, Qiuting Feng a, Jie Xu b, Teng Teng a, Qing Luan a, Congjia Shan a, Yali Hu b, Brian A. Hemmings c, Xiang Gao a, Zhongzhou Yang a,? a MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center of Nanjing University, Nanjing, China b Department of Obstetrics and Gynecology, Drum Tower Hospital, School of Medicine, Nanjing University, Nanjing, China c Friedrich Miescher Institute for Biomedical Research, Basel, Switzerland? Corresponding author. 12 Xuefu Road, Pukou, Nanjin E-mail address: zhongzhouyang@ (Z. Yan 0012-1606/$ – see front matter ? 2010 Elsevier Inc. Al doi:10.1016/j.ydbio.2010.08.033a b s t r a c ta r t i c l e i n f oArticle history: Received for publication 24 June 2010 Revised 16 August 2010 Accepted 26 August 2010 Available online 15 September 2010 Keywords: Akt/PKB knockout Heart defects p38 MAPKThe PI3K-PDK1-PKB/Akt (PI3K, phosphoinositide-3 kinase; PDK1, phosphoinositide-dependent protein kinase 1; PKB, protein kinase B) signaling pathway plays a critical role in a variety of biological processes including cell survival, growth and proliferation, metabolism and organogenesis. Previously, we generated Akt1-deficient mice and found high neonatal mortality with unknown causes. Here we report that histological analysis of Akt1-deficient embryos and newborns revealed heart defects and decreased cell proliferation. Echocardiographic study of Akt1-deficient mice indicated decreased heart function. Further investigation revealed that Akt1 deficiency caused substantial activation of p38MAPK in the heart. Breeding the Akt1- deficient mice to mice that were heterozygous for a null p38α partially rescued the heart defects, signific