ASIA unversity:Item 310904400/108089
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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/108089


    Title: Activation of IGF-I Survival Signaling and Its Compensative Inhibition of the Cardiac Apoptosis on Carotid Arteries Balloon-Injured Rat Hearts
    Authors: 謝承紘；Cheng-Hong Hsieh；Pei-Ying Pai；Pei-Ying Pai；Jia-Ping Wu；Jia-Ping Wu；Jia-Ping Wu；Jia-Ping Wu；Wu, Hsi-Chin；Wu,Hsi-Chin；Marthandam A；Marthandam Asokan Shibu；Cecilia Hsua；Cecilia Hsuan Day；Vijaya Padma；Vijaya Padma Viswanadha；Ho-Lin Chuan；Ho-Lin Chuang；黃志揚；Chih-yang Huang
    Contributors: 生物科技學系
    Date: 2017
    Issue Date: 2017-10-30 02:36:09 (UTC+0)
    Abstract: In this study, a rat carotid balloon injury-animal model was used to elucidate the temporal relation of hypertrophy in the progression of cardiac damage and the role of insulin-like growth factor (IGF)-I survival pathway on course of the cardiac damage. Rats were subjected to carotid balloon-injury and examined at different time points. We further studied the heart-weight/body-weight-ratio, histology and protein expression to understand the pathological events associated with percutaneous transluminal coronary angioplasty (PTCA) induced damages. Protein expression analysis showed increased levels of IGF-I signaling pathway and mitogen-activated protein kinase (MAPK) signaling pathway after 2 h and after 2 d of carotid balloon injury. On the other hand, apoptosis signaling pathways were enhanced after 14 d of carotid balloon injury. According to the results, rat carotid balloon injury significantly induced IGF-I survival signaling and compensated hypertrophy pathway during the initial period of injury however after 14 d the proteins involved in apoptotic cell death were elevated and the proteins of the survival pathway and compensatory hypertrophy were significantly reduced.

    KEYWORDS:
    cardiac apoptosis; compensated hypertrophy; decompensated hypertrophy; IGF-I survival pathway; percutaneous transluminal coronary angioplasty
    Relation: CHINESE JOURNAL OF PHYSIOLOGY
    Appears in Collections:[Department of Biotechnology] Journal Article

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