Can heat shock factor 1 be a novel target for vascular regeneration ?

我们使用 HSF1 敲除 (KO) 小鼠检查了 HSF1 是否通过动员和招募 BM 来源的干细胞/祖细胞来促进缺血诱导的血管生成。诱导缺血后，HSF1-KO小鼠缺血后肢的血流量和微血管密度显着低于野生型（WT）小鼠。缺血后，HSF1-KO 小鼠外周血中 BM 来源的 Sca-1 和 c-kit 阳性细胞的动员显着低于 WT 小鼠。与 WT 小鼠相比，HSF1-KO 小鼠的 BM 干/祖细胞向缺血组织的募集以及迁移、粘附和存活均显着减少。这些发现表明，HSF1 通过调节 BM 干细胞/祖细胞的动员和募集来促进缺血诱导的血管生成。

We examined whether HSF1 contributes to ischemia-induced angiogenesis through the mobilization and recruitment of BM-derived stem/progenitor cells using HSF1-knockout (KO) mice. After the induction of ischemia, blood flow and microvessel density in the ischemic hindlimb were significantly lower in the HSF1-KO mice than in the wild-type (WT) mice. The mobilization of BM-derived Sca-1- and c-kit-positive cells in peripheral blood after ischemia was significantly lower in the HSF1-KO mice than in the WT mice. BM stem/progenitor cells from HSF1-KO mice showed a significant decrease in their recruitment to ischemic tissue and in migration, adhesion, and survival when compared with WT mice. These findings suggest that HSF1 contributes to ischemia-induced angiogenesis by regulating the mobilization and recruitment of BM-derived stem/progenitor cells.