title: Short term triiodo-L-thyronine treatment inhibits cardiac myocyte apoptosis in border area after myocardial infarction in rats.
abstract: Thyroid hormone (TH) levels decline after a myocardial infarction (MI). Treatment with TH has been shown to improve left ventricular (LV) function in MI and other cardiovascular diseases, but the mechanisms are not clear. We have previously shown that TH can prevent myocyte apoptosis via Akt signaling in cultured neonatal rat cardiomyocytes. In this study, the effects of triiodo-L-thyronine (T3) on LV function and myocyte apoptosis after MI was examined in rats. After surgery, MI rats were treated with T3 for 3 days. Compared with sham-operated rats, MI rats showed significantly increased LV chamber dimension during systole and decreased LV function. T3 treatment increased LV +/-dP/dt but did not change LV chamber dimensions. MI rats also showed significantly increased myocyte apoptosis in the border area as assessed by DNA laddering and TUNEL assay. T3 treatment decreased the amount of DNA laddering, and reduced TUNEL positive myocytes in the border area, which was associated with phosphorylation of Akt at serine 473. These results suggest that T3 can protect myocytes against ischemia-induced apoptosis, which may be mediated by Akt signaling.
authors.affiliation: Cardiovascular Research Institute, Sanford Research/University of South Dakota, 1100 East 21st Street, Suite 700, Sioux Falls, SD 57105, USA.
authors.forename: Yue-Feng
authors.initials: YF
authors.lastname: Chen
authors.forename: Satoru
authors.initials: S
authors.lastname: Kobayashi
authors.forename: Jinghai
authors.initials: J
authors.lastname: Chen
authors.forename: Rebecca A
authors.initials: RA
authors.lastname: Redetzke
authors.forename: Suleman
authors.initials: S
authors.lastname: Said
authors.forename: Qiangrong
authors.initials: Q
authors.lastname: Liang
authors.forename: A Martin
authors.initials: AM
authors.lastname: Gerdes
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D001835:Body Weight / Q000187:drug effects; D004104:Diiodothyronines / Q000097:blood; D004789:Enzyme Activation / Q000187:drug effects; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000201:enzymology / Q000473:pathology*; D017202:Myocardial Ischemia / Q000517:prevention & control; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology*; D009929:Organ Size / Q000187:drug effects; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects; D013972:Thyrotropin / Q000097:blood; D013997:Time Factors; D014284:Triiodothyronine / Q000097:blood / Q000494:pharmacology*; D014463:Ultrasonography
chemical_list: D004104:Diiodothyronines; D014284:Triiodothyronine; D013972:Thyrotropin; D051057:Proto-Oncogene Proteins c-akt