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

我们利用HSF1基因敲除(KO)小鼠研究了HSF1是否通过动员和募集骨髓来源的干/祖细胞参与了缺血诱导的血管生成。在诱导缺血后，HSF1-KO小鼠缺血后肢的血流量和微血管密度显著低于野生型(WT)小鼠。HSF1-KO小鼠缺血后外周血中BM来源的SCA-1和c-kit阳性细胞的动员明显低于WT小鼠。与WT小鼠相比，HSF1-KO小鼠的BM干/祖细胞在缺血组织中的募集、迁移、黏附和存活显著减少。这些发现表明，HSF1通过调节骨髓来源的干/祖细胞的动员和募集，参与了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.