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This Article Full Text Full Text (PDF) All Versions of this Article: 293/3/H1766    most recent 00017.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Westberg, J. A. Articles by Andersson, L. C. Search for Related Content PubMed PubMed Citation Articles by Westberg, J. A. Articles by Andersson, L. C.

Hypoxic preconditioning induces elevated expression of stanniocalcin-1 in the heart

¹Department of Pathology, Haartman Institute, University of Helsinki and HUSLAB, Helsinki, Finland; and ²Department of Oncology and Pathology, Karolinska Institutet, Stockholm, Sweden

Submitted 5 January 2007 ; accepted in final form 11 June 2007

Animals exposed for a few hours to low oxygen content (8%) develop resistance against further ischemic myocardial damage. The molecular mechanism(s) behind this phenomenon, known as hypoxic preconditioning (HOPC), is still incompletely understood. Stanniocalcin-1 (STC-1) is an evolutionarily conserved glycoprotein originally discovered in fish, in which it regulates calcium/phosphate homeostasis and protects against toxic hypercalcemia. Our group originally reported expression of mammalian STC-1 in brain neurons and showed that STC-1 is a prosurvival factor that guards neurons against hypercalcemic and hypoxic damage. This study investigates the involvement of STC-1 in HOPC-induced cardioprotection. Wild-type mice and IL-6-deficient (Il-6^–/–) mice were kept in hypoxic conditions (8% O₂) for 6 h. Myocardial Stc-1 mRNA expression was quantified during hypoxia and after recovery. HOPC triggered a biphasic upregulation of Stc-1 expression in hearts of wild-type mice but not in those of Il-6^–/– mice. Treatment of cardiomyocyte cells in culture with hypoxia or IL-6 elicited an Stc-1 response, and ectopically expressed STC-1 in HL-1 cells localized to the mitochondria. Our findings indicate that IL-6-induced expression of STC-1 is one molecular mechanism behind the ischemic tolerance generated by HOPC in the heart.

cardioprotection; interleukin-6; mitochondria