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SelT exerts an essential cytoprotective action during development and after injury through its redox\u2010active catalytic site. This study aimed to determine the expression and regulation of SelT in the mammalian heart in normal and pathological conditions and to evaluate the cardioprotective effect of a SelT\u2010derived peptide, SelT43\u201052(<jats:styled-content style=\"fixed-case\">PSELT<\/jats:styled-content>) encompassing the redox motif which is key to its function, against ischaemia\/reperfusion(I\/R) injury.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We used the isolated Langendorff rat heart model and different analyses by immunohistochemistry, Western blot and <jats:styled-content style=\"fixed-case\">ELISA<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>We found that SelT expression is very abundant in embryo but is undetectable in adult heart. However, SelT expression was tremendously increased after I\/R. <jats:styled-content style=\"fixed-case\">PSELT<\/jats:styled-content> (5 nmol\/L) was able to induce pharmacological post\u2010conditioning cardioprotection as evidenced by a significant recovery of contractility (<jats:styled-content style=\"fixed-case\">dLVP<\/jats:styled-content>) and reduction of infarct size (<jats:styled-content style=\"fixed-case\">IS<\/jats:styled-content>), without changes in cardiac contracture (<jats:styled-content style=\"fixed-case\">LVEDP<\/jats:styled-content>). In contrast, a control peptide lacking the redox site did not confer cardioprotection. Immunoblot analysis showed that <jats:styled-content style=\"fixed-case\">PSELT<\/jats:styled-content>\u2010dependent cardioprotection is accompanied by a significant increase in phosphorylated Akt, Erk\u20101\/2 and Gsk3\u03b1\u2010\u03b2, and a decrement of p38<jats:styled-content style=\"fixed-case\">MAPK<\/jats:styled-content>. <jats:styled-content style=\"fixed-case\">PSELT<\/jats:styled-content> inhibited the pro\u2010apoptotic factors Bax, caspase 3 and cytochrome c and stimulated the anti\u2010apoptotic factor Bcl\u20102. Furthermore, <jats:styled-content style=\"fixed-case\">PSELT<\/jats:styled-content> significantly reduced several markers of I\/R\u2010induced oxidative and nitrosative stress.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>These results unravel the role of SelT as a cardiac modulator and identify <jats:styled-content style=\"fixed-case\">PSELT<\/jats:styled-content> as an effective pharmacological post\u2010conditioning agent able to protect the heart after ischaemic injury.<\/jats:p><\/jats:sec>","DOI":"10.1111\/apha.13067","type":"journal-article","created":{"date-parts":[[2018,3,25]],"date-time":"2018-03-25T18:57:06Z","timestamp":1522004226000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":69,"title":["A selenoprotein T\u2010derived peptide protects the heart against ischaemia\/reperfusion injury through inhibition of apoptosis and oxidative stress"],"prefix":"10.1111","volume":"223","author":[{"given":"C.","family":"Rocca","sequence":"first","affiliation":[{"name":"Laboratory of Cellular and Molecular Cardiovascular Physiology Department of Biology, Ecology and E.S. 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