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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 2016年第2期 8-8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 Noppmger Christian Grohe 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 *** 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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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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Abstracts from the 15th International Myopia Conference

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Eye and Vision 2016年第1期3卷 211-221页

作者： Alexandra Benavente-Perez Ann Nour Tobin Ansel Kathleen Abarr Luying Yan Keisha Roden David Troilo Chanyi Lu Miaozhen Pan Min Zheng Jia Qu Xiangtian Zhou Christine F. Wildsoet Fan Lu Jie Chen Jinhua Bao Liang Hu Qinmei Wang Zibing Jin Frances Rucker Stephanie Britton Stephan Hanowsky Molly Spatcher Hui-Ying Kuo Ching-Hsiu Ke I-Hsin Kuo Chien-Chun Peng Han-Yin Sun Ian G. Morgan Jeremy A. Guggenheim Rupal L. Shah Cathy Williams Jinglei Yang Peter S. Reinach Sen Zhang Wenfeng Sun Bo Liu Fen Li Xiaoqing Li Aihua Zhao Tianlu Chen Wei Jia Jun Jiang Haoran Wu Kazuo Tsubota Hiroko Ozawa Hidemasa Torii Shigemasa Takamizawa Toshihide Kurihara Kazuno Negishi klaus Graef Daniel Rathbun Frank Schaeffel Ladan Ghodsi William K. Stell Machelle T. Pardue Ranjay Chakraborty Han na Park Curran S. Sidhu P. Michael Iuvone Michael J Collins Nethrajeith Srinvasalu Sally A. McFadden Paul N. Baird Pablo Artal Pauline Cho SW Cheung Pei-Chang Wu Quan V. Hoang Duk C. Lee Erica G. Landis Michael A. Bergen Curran Sidhu Samer Hattar Richard A. Stone Ravi Metlapally Ruiqin Li Qinglin Xu Hong Zhong Chenglin Pan Weizhong Lan Xiaoning Li Ling Chen Zhikuan Yang Scott A. Read Seang-Mei Saw Shi-Jun Weng Xiao-Hua Wu Kang-Wei Qian Yun-Yun Li Guo-Zhong Xu Furong Huang Xiong-Li Yang Yong-Mei Zhong Earl L Smith, III Baskar Arumugam Li-Fang Hung Lisa A. Ostrin klaus Trier Monica Jong Brien A. Holden Thomas Chuen Lam Samantha Shan Bing Zuo Dennis Yan-yin Tse Jingfang Bian King-Kit Li Quan Liu Chi-ho To Timothy J. Gawne John T. Siegwart, Jr. Alexander H. Ward Thomas T. Norton Yan Zhang Yue Liu Carol Ho Eileen Phan Abraham Hang Emily Eng Christine Wildsoet Department of Biological Sciences SUNY College of Optometry New York NY 10036 USA School of Optometry and Ophthalmology and Eye Hospital Wenzhou Medical University Wenzhou Zhejiang 325027 China Center for Eye Disease & Development School of Optometry & Vision Science Program University of California Berkeley Berkeley CA 94720-2020 USA Wenzhou Medical University Wenzhou Zhejiang 325027 China Biomedical Science and Disease New England College of Optom Boston MA USA School of Optometry Chung Shan Medical University Taichung City 402 Taiwan Institute of Medicine Chung Shan Medical University Taichung City 402 Taiwan Division of Biochemistry and Molecular Biology Research School of Biology Australian National University Canberra Australia State Key Laboratory of Ophthalmology and Division of Preventive Ophthalmology Zhongshan Ophthalmic Center Sun Yat-Sen University Guangzhou China School of Optometry & Vision Sciences Cardiff University Cardiff UK School of Social and Community Medicine University of Bristol Bristol UK School of and Eye Hospital Wenzhou Medical University Wenzhou Zhejiang 325027 China State Key Laboratory Cultivation Base and Key Laboratory of Vision Science Ministry of Health and Zhejiang Provincial Key Laboratory of Ophthalmology and Optometry Wenzhou Zhejiang 325027 People’s Republic of China Shanghai Key Laboratory of Diabetes Mellitus and Center for Translational Medicine Shanghai Jiao Tong University Affiliated Sixth People’s Hospital Shanghai 200233 China Eye Hospital of Wenzhou Medical University Wenzhou Zhejiang 325027 China Department of Ophthalmology Keio University School of Medicine Shinjuku-ku Tokyo 160-8582 Japan General Medicine Ichikawa Medical Center Urayasu City Chiba 279-0001 Japan Ophthalmic Research Institute University of Tuebingen 72076 Tuebingen Germany Bernstein Center for Computational Neuroscience Tuebingen 72076 Tuebingen Germany Werner Reichardt Centre for Integrative Neuroscience Otfried-Mueller-Straße 25 Tueb

To assess the peripheral refractive changes that occur when eye growth decelerates in *** We measured peripheral refraction and on-axis vitreous chamber depth on a total of 53 marmosets;36 treated monocularly for 12 weeks 9 hrs/day(26 with-5 D contact lenses,10 with+5 D)and 17 untreated *** the 26 marmosets treated with-5 D,10 wore contact lenses 9 hrs/day without interruptions and were mea-sured at the end of 10 weeks of treatment(T10)and after 4 weeks of recovery(R14).Eight had both contact lenses removed for 30 mins twice/day(mid-morning and mid-afternoon)during the first four weeks of treatment(early interruption group)and eight had the lenses removed during the second four weeks of treatment(late interruption group).The two interruption groups were measured after 4,8 and 12 weeks of treatment only(T4,T8,T12).

关键词： removed treatment untreated

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