HIF-1 activation attenuates postischemic myocardial injury: role for heme oxygenase-1 in modulating microvascular chemokine generation.

@article{Ockaili2005HIF1AA,
  title={HIF-1 activation attenuates postischemic myocardial injury: role for heme oxygenase-1 in modulating microvascular chemokine generation.},
  author={Ramzi A Ockaili and Ramesh Natarajan and Fadi N. Salloum and Bernard J Fisher and Drew G. Jones and Alpha A Berry Fowler and Rakesh C. Kukreja},
  journal={American journal of physiology. Heart and circulatory physiology},
  year={2005},
  volume={289 2},
  pages={
          H542-8
        }
}
The CXC chemokine IL-8, which promotes adhesion, activation, and transmigration of polymorphonuclear neutrophils (PMN), has been associated with production of tissue injury in reperfused myocardium. Hypoxia-inducible factor-1 (HIF-1) is a heterodimeric peptide that is a key regulator of genes such as heme oxygenase (HO)-1 expressed under hypoxic conditions. We hypothesized that HO-1 plays an important role in regulating proinflammatory mediator production under conditions of ischemia… 
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An updated overview on the involvement of HIF-1 in the induction of cardioprotective molecules, such as inducible nitric oxide synthase, hemeoxygenase 1 (HO-1), and erythropoietin (EPO), which in turn alleviate myocardial damages caused by harmful events such as ischemia-reperfusion injury is provided.
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In vitro and in vivo, PHD2 silencing using a siRNA strategy produces transcriptionally active HIF-1, which attenuates reperfusion injury via an iNOS-dependent pathway and stabilization in normoxia murine microvascular endothelial cells.
Hypoxia inducible factor-1α contributes to UV radiation-induced inflammation, epidermal hyperplasia and immunosuppression in mice.
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  • Biology, Medicine
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  • 2012
TLDR
It is demonstrated that HIF-1α protein is an early responder to UV radiation in the skin, and its activation can be attenuated by treating mice with its post-translational inhibitor, YC-1, following UV-irradiation of mice.
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