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. 2007 Feb;190(2):321-9.
doi: 10.1016/j.atherosclerosis.2006.03.037. Epub 2006 May 5.

HSF1 and constitutively active HSF1 improve vascular endothelial function (heat shock proteins improve vascular endothelial function)

Tsuyoshi Uchiyama  1 , Hiroyuki Atsuta, Toshihiro Utsugi, Masato Oguri, Akira Hasegawa, Tetsuya Nakamura, Akira Nakai, Masanori Nakata, Ikuro Maruyama, Hideaki Tomura, Fumikazu Okajima, Shoichi Tomono, Shoji Kawazu, Ryozo Nagai, Masahiko Kurabayashi
Affiliations

HSF1 and constitutively active HSF1 improve vascular endothelial function (heat shock proteins improve vascular endothelial function)

Tsuyoshi Uchiyama et al. Atherosclerosis. 2007 Feb.

Abstract

We have been examining the role of heat shock factor 1 (HSF1) in the pleiotropic effects of statins. In parallel studies, we found that statin induces the nuclear translocation of HSF1 and that a decoy oligonucleotide encoding the heat shock element inhibits the statin-induced expression of heat shock protein 70, endothelial nitric oxide synthase (eNOS) and thrombomodulin. Also, in vascular endothelial cells, increases in the expression of human HSF1 corresponded with elevated steady-state levels of eNOS and thrombomodulin and reduced levels of endothelin-1 and plasminogen activator inhibitor-1. We also found that heat shock proteins induced eNOS and thrombomodulin expression and reduced PAI-1 and ET-1 expression. In particular, a combination of HSP70 and HSP90 strongly induced eNOS expression and reduced PAI-1 expression. In the current studies, we generated a constitutively active form of HSF1 and found that it is more effective than the wild-type HSF at inducing thrombomodulin and eNOS expression and decreasing endothelin-1 and plasminogen activator inhibitor-1 expression. These results show that the wild-type and constitutively active forms of HSF1 induce anticoagulation and relaxation factors in vascular endothelial cells and could therefore be used to treat cardiovascular disease.

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