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The study for the mechanism of loss of hair after the transient ischemia

短暂性脑缺血后脱发机制的研究

基本信息

批准号：
18591962
负责人：
IMAI Yoshimichi
金额：
$ 2.44万
依托单位：
Tohoku University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2006
资助国家：
日本
起止时间：
2006 至 2007
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-18591962/
关键词：
ischemia reperfusin keratinocyte hair follicle 72kd-Heat Shock Protein apoptosis molecular chaperone caspase-3 深部毛包細胞浅部毛包細胞虚血耐性皮弁 72kd-heat shock protein 虚血性脱毛

项目摘要

Seventy-two-kd heat-shock protein (HSP72) is one of the stress markers induced in cells under stress, such as in the case of ischemia. Recent studies have suggested that HSP72 is a "molecular chaperone" to protect cells from various kinds of stress, and that the temporal profile of HSP72 induction is related to ischemic vulnerability. In this study, we attempted to analyze the temporal profiles of HSP72 induction in keratinocytes in the shallow hair follicles and the deep hair follicles in skin flaps after various periods of transient ischemia, and we investigated the reason why there were differences in ischemic tolerance between these cells.We used the abdominal skin flap of Wister rats, which were divided into three groups: the sham control group (n=27), the 2-hour ischemia group (n=25), and the 8-hour ischemia group (n=25). At periods of 8, 24, 48, 96 hours, and 7 days after reperfusion, we examined them for any histological changes and performed immunostaining for HSP72 and caspas … More e-3 (n=5, each time point). In addition, we performed TUNEL stain for detecting apoptosis.As a result, the keratinocytes in the shallow hair follicles in all groups revealed positive for HSP72 through the time course, regardless of the ischemic stresses, and they were not positive for TUNEL stain. In the deep hair follicles, the cells in the sham control group revealed no immunoreactivity after the reperfusion, and they had no positive cell in TUNEL stain. In the 2-hour ischemia group, the keratinocytes gradually increased the reactivity for HSP72; consequently they also had no positive cell in TUNEL stain at all. In the 8-hour ischemia group, the reactivity for HSP72 was revealed at 8 hours after the reperfusion and suddenly decreased at 24 hour after the reperfusion; consequently they revealed positive for TUNEL stain. And they also expressed active form of caspase-3 at 8 hours after the reperfusion.We concluded that these differences of HSP72 expression were related to the deep follicle''s vulnerability to ischemia. The 8-hour ischemia induced the disturbance of HSP72 induction only in the deep hair follicles, consequently the keratinocytes in the deep hair follicles revealed apoptosis. And this apoptosis was accompanied with the activation of caspase-3. Less

72kd的热休克蛋白(HSP72)是细胞在应激状态下诱导的应激标志物之一，如在缺血情况下。最近的研究表明，HSP72是一种分子伴侣，可以保护细胞免受各种应激的影响，并且HSP72诱导的时间分布与缺血易感性有关。本研究以Wistar大鼠腹壁皮瓣为实验模型，随机分为假手术对照组(n=27)、缺血2小时组(n=25)和缺血8小时组(n=25)，分析短暂性脑缺血不同时期浅层毛囊和深层毛囊角质形成细胞HSP72诱导表达的时间变化规律，并探讨其在缺血耐受性上存在差异的原因。在再灌注后8、24、48、96小时和7天，我们检查它们的组织学变化，并进行hsp72和caspas…的免疫组织化学染色。更多e-3(n=5，每个时间点)。此外，我们还进行了TUNEL染色，结果显示，无论缺血应激程度如何，所有组浅层毛囊中的角质形成细胞均呈HSP72阳性，而TUNEL染色均为阴性。在深层毛囊中，假手术组再灌注后未见免疫反应阳性细胞，TUNEL染色未见阳性细胞。在缺血2小时组，角质形成细胞对HSP72的反应性逐渐增强，TUNEL染色也未见阳性细胞。在缺血8h组，HSP72在再灌流后8h出现阳性反应，再灌流后24h突然下降，TUNEL染色呈阳性。结论：HSP72表达的差异与深层毛囊对缺血的易感性有关，缺血8h仅在深层毛囊诱导HSP72诱导紊乱，从而导致深部毛囊角质形成细胞发生凋亡，而这种凋亡伴随着caspase-3的激活。