Seventy-two-kd heat-shock protein (HSP72) is one of the stress markers induced in cells under stress, such as in the case of ischaemia. 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 ischaemic vulnerability. In this study, we attempted to analyse the temporal profiles of HSP72 induction in epithelial and adipose cells in skin flaps after various periods of transient ischaemia, and we investigated the reason why there were differences in ischaemic 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-h ischaemia group (n=25), and the 8-h ischaemia group (n=25). At periods of 8, 24, 48, 96 h, and 7 days after reperfusion, we examined them for any histological changes and performed immunostaining for HSP72 (n=5, each time point). Two animals in the sham control group were sacrificed to harvest the samples immediately after the skin flaps were elevated. As a result, the epithelial cells in all groups revealed positive for HSP72 through the time course, regardless of the ischaemic stresses, and they were alive at 7 days. In the adipose cells, the cells in the sham control group revealed no immunoreactivity after the reperfusion, and they had no change at 7 days. In the 2-h ischaemia group, the adipose cells gradually increased the reactivity for HSP72; consequently they survived beyond 7 days. In the 8-h ischaemia group, the reactivity for HSP72 gradually decreased; consequently they played out a delayed cell death at 7 days. We concluded that these differences of HSP72 expression were related to the cellular vulnerability to ischaemia.
|ジャーナル||Journal of Plastic, Reconstructive and Aesthetic Surgery|
|出版ステータス||Published - 2006 3月|
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