Differential induction of HSP60 and HSP72 by different stress situations in rats - Correlation with cerulein-induced pancreatitis
Differential induction of HSP60 and HSP72 by different stress situations in rats - Correlation with cerulein-induced pancreatitis
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DOI：
10.1023/a:1018866727129
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发表时间：
1997-07-01
影响因子：
3.1
通讯作者：
Masamune, O
中科院分区：
文献类型：
--
作者：
Otaka, M;Okuyama, A;Masamune, O
我们之前报道过，水浸应激特异性诱导胰腺细胞合成60 kda的热休克蛋白（HSP60，伴侣蛋白同源物），预诱导HSP60以定量依赖的方式完全阻止cerulein诱导的大鼠胰腺炎的发展。为了研究72 kda热休克蛋白（HSP72，应激诱导型hsp70）的细胞保护功能，本研究通过热疗特异性预诱导HSP72对cerulein诱导的胰腺炎的影响，并与预诱导HSP60的效果进行比较。采用免疫印迹法检测浸泡和热疗前后胰腺组织中HSP60和HSP72的表达。经水浸应激或热休克预处理后，大鼠腹腔注射丙核蛋白（40 μ g/kg）。测定注射蓝蛋白前后胰腺湿重和血清淀粉酶浓度。高温（42.5℃，20分钟）在胰腺特异性诱导HSP72。水浸应激在胰腺中特异性诱导HSP60的合成。水浸应激特异性预诱导HSP60可明显预防蓝蛋白诱导的胰腺炎。然而，热疗预诱导HSP72对冠状蛋白诱导的胰腺炎没有预防作用。我们的研究结果表明，HSP60和HSP72在胰腺中具有不同的功能，它们在体内的诱导机制也不同。这些结果可能对理解热休克蛋白介导的胰腺“适应性细胞保护”机制具有重要意义。
We previously reported that water-immersion stress specifically induced the synthesis df a 60-kDa heat-shock protein (HSP60, chaperonin homolog) in pancreatic cells and preinduction of HSP60 completely prevented development of cerulein-induced pancreatitis in the rat in an HSP60 quantitatively dependent manner. In order to study the cytoprotective function of a 72-kDa heat-shock protein (HSP72, stress-inducible hsp70), the effect of specific preinduction of HSP72 by hyperthermia on cerulein-induced pancreatitis was investigated and compared with the effect of preinduction of HSP60 in this study. Expression of HSP60 and HSP72 in the pancreas was investigated by immunoblot before and after water immersion or hyperthermia. Following pretreatment with water-immersion stress or hyperthermia, the rats were injected with cerulein (40 mu g/kg, intraperitoneally). The pancreas wet weight and serum amylase concentration were measured before and after cerulein injection. Hyperthermia (42.5 degrees C, 20 min) specifically induced HSP72 in the pancreas. The synthesis of HSP60 was specifically induced by water-immersion stress in the pancreas. Cerulein-induced pancreatitis was clearly prevented by specific preinduction of HSP60 by water-immersion stress. However, preinduction of HSP72 by hyperthermia had no preventive effect on cerulein-induced pancreatitis. Our findings suggest that HSP60 and HSP72 have distinct functions in the pancreas, and their induction mechanisms are also different in vivo. These results could be important for understanding the mechanism of ''adaptive cytoprotection'' in the pancreas mediated by heat-shock proteins.