Literature DB >> 19176596

Cardioprotection by hypoxia-inducible factor 1 alpha transfection in skeletal muscle is dependent on haem oxygenase activity in mice.

Gabor Czibik1, Julia Sagave, Vladimir Martinov, Bushra Ishaq, Marcus Sohl, Iren Sefland, Harald Carlsen, Filip Farnebo, Rune Blomhoff, Guro Valen.   

Abstract

AIMS: The present study investigates whether the cardioprotection achieved by gene delivery of hypoxia-inducible factor-1 alpha (HIF-1 alpha) depends on the downstream factor haem oxygenase (HMOX)-1. METHODS AND
RESULTS: Immortalized cardiomyocytes (HL-1 cells) were transfected with HIF-1 alpha or HMOX-1 and injured with hydrogen peroxide (H(2)O(2)), and death was evaluated by trypan blue staining. Quadriceps muscles of mice were treated with DNA for HIF-1 alpha and HMOX-1, or sham-treated and electroporated, and 3 days later, hearts were isolated and subjected to global ischaemia and reperfusion. Some HIF-1 alpha- and sham-treated mice received the HMOX blocker zinc deuteroporphyrin 2,4-bis-glycol (ZnBG) (n = 6-8 in each group). HL-1 cells were stimulated with bilirubin or the carbon monoxide donor CORM-2 before injury with H(2)O(2). HL-1 cells which were transfected with HIF-1 alpha or HMOX-1 had an increased survival to H(2)O(2)-induced injury compared with empty vector (n = 10-12 per group; P < 0.01 for both). When HMOX-1-luciferase reporter mice were treated with HIF-1 alpha in the quadriceps muscle, increased luciferase activity was found locally, but nowhere else. Mice pre-treated with HIF-1 alpha or HMOX-1 had a reduced infarct size, improved post-ischaemic function, and increased serum bilirubin (P < 0.05). ZnBG inhibited all these effects afforded by HIF-1 alpha. Stimulation of HL-1 cells with bilirubin and CORM-2 reduced cell death evoked by H(2)O(2) (P < 0.05 for both, n = 11-15 in each group).
CONCLUSION: HIF-1 alpha and HMOX-1 provided protection against H(2)O(2)-induced damage in HL-1 cells. Remote gene delivery of HIF-1 alpha afforded cardioprotective effects. These were dependent on HMOX activity, as an HMOX blocker abolished the effects, and they were mimicked by pre-treatment with HMOX-1. Downstream to HMOX-1, bilirubin as well as carbon monoxide may be organ effectors.

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Year:  2009        PMID: 19176596     DOI: 10.1093/cvr/cvp035

Source DB:  PubMed          Journal:  Cardiovasc Res        ISSN: 0008-6363            Impact factor:   10.787


  12 in total

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