title: Adaptational changes of MHC gene expression and isozyme transition in cardiac overloading.
abstract: Distribution of cardiac myosin heavy-chain (MHC) isozymes is regulated during development by hemodynamic change and hormonal stimuli. To understand the evolution of cardiac hypertrophy and the underlying processes, the interaction between acute or chronic cardiac over-loading and serum thyroid hormone levels was studied. Biochemical, physiological, and pathological studies were performed using coarctated (Coa) rats with or without administration of thyroid hormone (Thy) and on sham-operated (Sham) rats and normal rats with or without administration of Thy. The results showed that 1) although serum Thy levels in Coa and Sham rats were nearly the same at all timing points, a significant induction of beta-MHC mRNA and isozyme occurred in Coa rats; 2) in Coa rats where Thy was administered, there was no increase in beta-MHC mRNA and isozyme as seen in Coa rats, and this level was nearly the same as in Sham rats, whereas serum Thy levels were significantly high, as in the normals with administration of Thy; and 3) 77 days after surgery, the hypertrophy was completed, judging from pathological findings at this time, and beta-MHC mRNA and isozyme reached similar levels in all groups, except for the normals with administration of Thy. These results demonstrate the following: 1) the MHC isoform transitions induced by pressure overload are not induced by decreases in serum Thy levels, and the regulation of MHC gene expression is responsive to other triggers in addition to Thy; and 2) the first adaptational process of the heart to hemodynamic overload is the MHC isoform transition, and the second adaptational process of that is the hypertrophy itself.
authors.affiliation: Research Division Heart Institute of Japan, Tokyo.
authors.forename: S
authors.initials: S
authors.lastname: Imamura
authors.forename: R
authors.initials: R
authors.lastname: Matsuoka
authors.forename: E
authors.initials: E
authors.lastname: Hiratsuka
authors.forename: M
authors.initials: M
authors.lastname: Kimura
authors.forename: T
authors.initials: T
authors.lastname: Nakanishi
authors.forename: T
authors.initials: T
authors.lastname: Nishikawa
authors.forename: Y
authors.initials: Y
authors.lastname: Furutani
authors.forename: A
authors.initials: A
authors.lastname: Takao
mesh_terms: D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D006332:Cardiomegaly / Q000378:metabolism*; D015870:Gene Expression; D006321:Heart / Q000187:drug effects / Q000502:physiology; D006439:Hemodynamics / Q000502:physiology; D008297:Male; D008854:Microscopy, Electron; D009206:Myocardium / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D009218:Myosins / Q000235:genetics* / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D013963:Thyroid Hormones / Q000097:blood / Q000502:physiology
chemical_list: D012333:RNA, Messenger; D013963:Thyroid Hormones; D000251:Adenosine Triphosphatases; D009218:Myosins