title: Abnormal immunostaining for dystrophin in isoproterenol-induced acute myocardial injury in rats: evidence for change in dystrophin in the absence of genetic defect.
abstract: Abnormalities in the gene for Duchenne muscular dystrophy produce skeletal and myocardial changes, by impairing dystrophin production in patients with Duchenne and Becker muscular dystrophy. However, it is not known whether myocardial dystrophin may be altered in patients with other heart diseases. To investigate whether changes in myocardial dystrophin may be induced by acute myocardial injury, the immunostaining patterns of myocardial dystrophin were examined, together with those of myocardial actin, in rats with isoproterenol-induced myocardial damage. Hearts were excised at 6, 12, 24 and 48 h, and 1 and 4 weeks after the subcutaneous administration of 100 mg/kg of isoproterenol. Frozen serial sections were prepared for haematoxylin and eosin staining, and for immunostaining for dystrophin and actin. The immunostaining patterns of actin were used as an indicator of cell injury. The myocardial cells observed were classified into four types, according to staining pattern: normal for both actin and dystrophin (Type 1): normal for actin, but abnormal for dystrophin (Type 2); abnormal for actin, but normal for dystrophin (Type 3); and abnormal for both actin and dsytrophin (Type 4). The percentage of myocardial cells with abnormal staining (Types 2, 3 and 4) at 6, 12, 24 and 48 h after isoproterenol injection was 22.4, 12.6, 16.0 and 2.4%, respectively; most cells were Types 3 and 4. One week after injection or later, no Type 3 or 4 cells were detected, while the percentages of Type 2 cells were 2.7% for 1 week and 2.2% for 4 weeks, significantly higher than the corresponding value in the control group. In conclusion, changes in myocardial dystrophin may occur in isoproterenol-induced myocardial injury in rats.
authors.affiliation: The First Department of Internal Medicine, Faculty of Medicine, Kagoshima University, Sakuragaoka, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Miyazato
authors.forename: S
authors.initials: S
authors.lastname: Biro
authors.forename: M
authors.initials: M
authors.lastname: Setoguchi
authors.forename: M
authors.initials: M
authors.lastname: Maeda
authors.forename: T
authors.initials: T
authors.lastname: Tashiro
authors.forename: S
authors.initials: S
authors.lastname: Nakao
authors.forename: H
authors.initials: H
authors.lastname: Tanaka
mesh_terms: D000199:Actins / Q000276:immunology / Q000378:metabolism; D000818:Animals; D002316:Cardiotonic Agents / Q000633:toxicity; D003593:Cytoplasm / Q000473:pathology; D016189:Dystrophin / Q000235:genetics* / Q000276:immunology*; D004487:Edema / Q000473:pathology; D004801:Eosine Yellowish-(YS) / Q000737:chemistry; D006331:Heart Diseases / Q000473:pathology; D006335:Heart Injuries / Q000139:chemically induced / Q000378:metabolism*; D007150:Immunohistochemistry; D007545:Isoproterenol / Q000633:toxicity*; D008297:Male; D009206:Myocardium / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar
chemical_list: D000199:Actins; D002316:Cardiotonic Agents; D016189:Dystrophin; D007545:Isoproterenol; D004801:Eosine Yellowish-(YS)