Laboratory Animal and Comparative Medicine ›› 2014, Vol. 34 ›› Issue (3): 181-186.DOI: 10.3969/j.issn.1674-5817.2014.03.003

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Changes of PKCβII Protein Expression and Membrane Translocation in Pulmonary Artery of Rats with Hypoxic Pulmonary Hypertension

GUO Wan-jin1, SHI Yi-wei2, ZHANG Ai-zhen1, DU Yong-cheng1   

  1. 1. Department of Respiratory Medicine, People's Hospital of Shan Xi Medical University, Taiyuan 030001, China;
    2. Department of Respiratory Medicine, the First Hospital of Shan Xi Medical University, Taiyuan 030001, China
  • Received:2013-10-18 Online:2014-06-25 Published:2014-06-25

Abstract: Objective To establish rats model of chronic pulmonary hypertension (PH) and preliminarily explore the effect of PKCâII in the development of hypoxia-induced pulmonary hypertension. Methods Male SD rats were exposed to normobaric hypoxia to induce PH model. The rats were randomly divided into six groups, and exposed to normoxia control and to normoxia hypoxia for 1 d, 3 d, 7 d, 14 d and 21 d. Right ventricle systolic pressure (RVSP) and right ventricle hypertrophy index(RVHI) were measured. Pathological changes of the pulmonary arteries were observed by HE staining. The changes of PKCβII protein expression and membrane translocation in pulmonary arteries were also detected by Western blotting. Results RVSP increased significantly after hypoxic exposure for 1 d, 3 d, 7 d, 14 d and 21 d when compared with the normoxia control(P<0.05); There were significant rise in RVHI after hypoxic exposure for 3 d, 7 d, 14 d and 21 d (P<0.05). The pathological changes of the pulmonary arteries were significant at 3 d, 7 d, 21 d. PKCâII protein expression decreased significantly at 3 d, 7 d, 14 d, 21 d after chronic hypoxia than those of normal control groups respectively(P<0.05). Significant decrease of PKCβII membrane translocation level in pulmonary arteries of rats could be detected after hypoxic exposure 3 d(P<0.05). Conclusion The decrease in protein expression and membrane translocation of PKCβII may be involved in the development of the chronic hypoxia-induced pulmonary hypertension.

Key words: Protein kinase CβII, Chronic hypoxia, Pulmonary hypertension, Membrane translocation, Protein expression

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