Lin Lung-Chang, Chen Hsiang-Wen, Yang Rei-Cheng
Department of Pediatrics, Kaohsiung Municipal Hsiao Kang Hospital, Taiwan.
Kaohsiung J Med Sci. 2005 Mar;21(3):101-7. doi: 10.1016/S1607-551X(09)70285-2.
The pathophysiology of febrile convulsion, the most common childhood neurologic disease, remains unclear. In this study, we investigated what role a heat shock protein plays in this disease. We enrolled eight boys and two girls with febrile convulsion and 10 age-matched healthy controls. We did a biosynthetic evaluation of both groups by separating lymphocytes and measuring the expression of heat shock protein 72 before and after heat shock treatment. Before the treatment, both groups were found to have small amounts of constitutive heat shock protein 72. Afterwards, its expression increased in both groups, and no statistical difference was found between the increases in the two groups. In addition, there was no obvious difference in the susceptibility to produce heat shock proteins. However, the febrile convulsion group was found to have a significant decrease in phosphorylation of heat shock protein 72. These results suggest the possible involvement of post-translational modification of heat shock proteins, most likely phosphorylation, in the pathogenesis of febrile convulsion.
热性惊厥是最常见的儿童神经系统疾病,其病理生理学仍不清楚。在本研究中,我们调查了热休克蛋白在该疾病中所起的作用。我们招募了8名患热性惊厥的男孩和2名女孩以及10名年龄匹配的健康对照。通过分离淋巴细胞并测量热休克处理前后热休克蛋白72的表达,我们对两组进行了生物合成评估。治疗前,两组均发现有少量组成型热休克蛋白72。之后,两组中其表达均增加,两组增加量之间未发现统计学差异。此外,产生热休克蛋白的易感性没有明显差异。然而,发现热性惊厥组中热休克蛋白72的磷酸化显著降低。这些结果表明热休克蛋白的翻译后修饰,最有可能是磷酸化,可能参与了热性惊厥的发病机制。