Immunohistochemical localization of mitogen-activated protein kinase (MAPK) family and morphological changes in rat heart after ischemia-reperfusion injury

被引:13
作者
Naito Z. [1 ]
Kudo M. [1 ]
Xu G. [1 ]
Nishigaki R. [1 ]
Yokoyama M. [1 ]
Yamada N. [1 ]
Asano G. [1 ]
机构
[1] Department of Pathology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku
来源
Medical Electron Microscopy | 2000年 / 33卷 / 2期
关键词
Heart; Immunohistochemistry; Ischemia reperfusion injury; Mitogen-activated protein kinase (MAPK); Ultrastructure;
D O I
10.1007/s007950070005
中图分类号
学科分类号
摘要
The mitogen-activated protein kinase (MAPK) family is considered to be activated by stress, but the role of the MAPK family is still unknown in cardiac pathology. In the present study, not only the localization of MAPKs such as the extracellular responsive kinase (ERK), c-jun N-terminal kinase (JNK), and p38 MAPK (p38), but also ultrastructural changes were investigated in the ischemia-reperfusion model of Wistar rats. At 5, 10, 30, 60, and 180min reperfusion after 30 min ischemia by occluding the coronary artery, the expression of these MAPKs was increased in blood vessels and cardiomyocytes by Western blotting and immunohistochemical methods. In addition, after ischemia reperfusion, various ultrastructural changes such as decreased glycogen granules, mitochondrial swelling, and myolysis were observed in the blood vessels and cardiomyocytes. These results suggest that protein kinases may regulate numerous biological processes, including the regulation of contraction and ion transport.
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页码:74 / 81
页数:7
相关论文
共 26 条
[1]  
Asano, G., Oguro, T., Hirohata, Y., Schwartz, A., The effects of early ischemia on dog heart: Ultrastructural study (1980) J Clin Electron Microsc, 13, pp. 5-6
[2]  
Ishiharajima, S., Aida, T., Nakagawa, R., Kameyama, K., Sugano, K., Oguro, T., Asano, G., Early membrane damage during ischemia in rat heart (1986) Exp Mol Pathol, 44, pp. 1-6
[3]  
Cowan, M.J., Reichenbach, D., Turner, P., Thostenson, C., Cellular response of the evolving myocardial infarction after therapeutic coronary artery reperfusion (1991) Hum Pathol, 22, pp. 154-163
[4]  
Cook, S.A., Sugden, P.H., Clerk, A., Activation of c-Jun N-terminal kinases and p38-mitogen-activated protein kinases in human heart failure secondary to ischaemic heart disease (1999) J Mol Cell Cardiol, 31, pp. 1429-1434
[5]  
Omura, T., Yoshiyama, M., Shimada, T., Shimizu, N., Kim, S., Iwao, H., Takeuchi, K., Yoshikawa, J., Activation of mitogen-activated protein kinases in in vivo ischemia/reperfused myocardium in rats (1999) J Mol Cell Cardiol, 31, pp. 1269-1279
[6]  
Bradford, M.M., A rapid sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding (1976) Anal Biochem, 72, pp. 248-254
[7]  
Benjamin, I.J., McMilan, D.R., Stress (heat shock) proteins: Molecular chaperones in cardiovascular biology and disease (1998) Circ Res, 83, pp. 117-132
[8]  
Hirai, K., Ashraf, M., Modulation of adenosine effects in attenuation of ischemia and reperfusion injury in rat heart (1998) J Mol Cell Cardiol, 30, pp. 1803-1815
[9]  
Takashi, E., Pathologic assessment of myocardial cell necrosis and apoptosis after ischemia and reperfusion with molecular and morphological markers (2000) J Mol Cell Cardiol, 32, pp. 209-224
[10]  
Sugden, P.H., Bogoyevitch, M.A., Intracellular signalling through protein kinases in the heart (1995) Cardiovasc Res, 218, pp. 83-88