title: Alteration of serum and cardiac tissue adropin, copeptin, irisin and TRPM2 expressions in DOX treated male rats.
abstract: Doxorubicin (DOX) cardiotoxicity is a significant side effect in cancer survivors. DOX and its metabolites alter cardiac gene expression and affect metabolic energy-related peptides. Adropin, copeptin, irisin and TRPM2 are produced locally in the heart and play a role in energy homeostasis. We investigated the fates of adropin, copeptin, irisin and TRPM2 in serum and cardiac tissues of DOX treated rats. Animals were divided into three groups of six: 1) untreated controls, 2) DOX treated and 3) saline treated. The rats were fed a standard diet ad libitum for 14 days then were sacrificed and heart and serum samples were taken. Adropin, copeptin, irisin levels in tissue homogenates and serum were measured using ELISA. Immunoreactivity of heart tissue adropin, copeptin, irisin and TRPM2 also were investigated. The peptides increased in both serum and cardiac tissue homogenates in animals treated with DOX compared to the other groups. DOX increased adropin in endocardial and myocardial cells, but it decreased expression of copeptin. DOX did not affect endocardial irisin and TRPM2 expressions, but myocardial irisin and TRPM2 expressions were increased. Serum adropin, irisin and copeptin were increased in DOX treated rats. Cardiac adropin, copeptin, irisin and TRPM2 are affected by DOX and may play a role in DOX cardiotoxicity.
authors.affiliation: Elazig Education and Research Hospital, Clinic of Cardiovascular Surgery , Elazig, 23119.
authors.forename: S
authors.initials: S
authors.lastname: Aydin
authors.forename: M N
authors.initials: MN
authors.lastname: Eren
authors.forename: T
authors.initials: T
authors.lastname: Kuloglu
authors.forename: S
authors.initials: S
authors.lastname: Aydin
authors.forename: M
authors.initials: M
authors.lastname: Yilmaz
authors.forename: E
authors.initials: E
authors.lastname: Gul
authors.forename: M
authors.initials: M
authors.lastname: Kalayci
authors.forename: Y
authors.initials: Y
authors.lastname: Yel
authors.forename: T
authors.initials: T
authors.lastname: Cakmak
authors.forename: S
authors.initials: S
authors.lastname: Bico
mesh_terms: D000818:Animals; D000903:Antibiotics, Antineoplastic / Q000633:toxicity*; D001798:Blood Proteins / Q000378:metabolism*; D004317:Doxorubicin / Q000633:toxicity*; D005353:Fibronectins / Q000097:blood / Q000378:metabolism*; D006020:Glycopeptides / Q000097:blood / Q000378:metabolism*; D006321:Heart / Q000187:drug effects; D006331:Heart Diseases / Q000139:chemically induced / Q000378:metabolism; D007150:Immunohistochemistry; D008297:Male; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D010455:Peptides / Q000097:blood / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D050053:TRPM Cation Channels / Q000378:metabolism*
chemical_list: D000903:Antibiotics, Antineoplastic; D001798:Blood Proteins; C586182:ENHO protein, rat; C583676:FNDC5 protein, rat; D005353:Fibronectins; D006020:Glycopeptides; D010455:Peptides; D050053:TRPM Cation Channels; C557080:Trpm2 protein, rat; C048197:copeptins; D004317:Doxorubicin
keywords: TRPM2; adropin; cardiac tissue; copeptin; doxorubicin; irisin