title: The profile of cardiac cytochrome c oxidase (COX) expression in an accelerated cardiac-hypertrophy model.
abstract: The contribution of the mitochondrial components, the main source of energy for the cardiac hypertrophic growth induced by pressure overload, is not well understood. In the present study, complete coarctation of abdominal aorta was used to induce the rapid development of cardiac hypertrophy in rats. One to two days after surgery, we observed significantly higher blood pressure and cardiac hypertrophy, which remained constantly high afterwards. We found an early increased level of cytochrome c oxidase (COX) mRNA determined by in-situ hybridization and dot blotting assays in the hypertrophied hearts, and a drop to the baseline 20 days after surgery. Similarly, mitochondrial COX protein level and enzyme activity increased and, however, dropped even lower than baseline 20 days following surgery. In addition, in natural hypertension-induced hypertrophic hearts in genetically hypertensive rats, the COX protein was significantly lower than in normotensive rats. Taken together, the lower efficiency of mitochondrial activity in the enlarged hearts of long-term complete coarcted rats or genetically hypertensive rats could be, at least partially, the cause of hypertensive cardiac disease. Additionally, the rapid complete coarctation-induced cardiac hypertrophy was accompanied by a disproportionate COX activity increase, which was suggested to maintain the cardiac energy-producing capacity in overloaded hearts.
authors.affiliation: Institute of Biochemistry, Chung-Shan Medical University, Taichung, Taiwan, ROC.
authors.forename: Wei-Wen
authors.initials: WW
authors.lastname: Kuo
authors.forename: Chia-Yih
authors.initials: CY
authors.lastname: Chu
authors.forename: Chieh-Hsi
authors.initials: CH
authors.lastname: Wu
authors.forename: James A
authors.initials: JA
authors.lastname: Lin
authors.forename: Jer-Yuh
authors.initials: JY
authors.lastname: Liu
authors.forename: Tsung-Ho
authors.initials: TH
authors.lastname: Ying
authors.forename: Shin-Da
authors.initials: SD
authors.lastname: Lee
authors.forename: Yi-Hsien
authors.initials: YH
authors.lastname: Hsieh
authors.forename: Chu-Hsien
authors.initials: CH
authors.lastname: Chu
authors.forename: Ding-Yu
authors.initials: DY
authors.lastname: Lin
authors.forename: Hsi-Hsien
authors.initials: HH
authors.lastname: Hsu
authors.forename: Chih-Yang
authors.initials: CY
authors.lastname: Huang
mesh_terms: D000818:Animals; D015153:Blotting, Western; D001835:Body Weight; D003576:Electron Transport Complex IV / Q000096:biosynthesis* / Q000737:chemistry / Q000378:metabolism / Q000502:physiology*; D005263:Femoral Artery / Q000473:pathology; D015870:Gene Expression; D006973:Hypertension / Q000473:pathology*; D006984:Hypertrophy / Q000473:pathology*; D017379:Hypertrophy, Left Ventricular / Q000473:pathology; D017403:In Situ Hybridization; D008297:Male; D008928:Mitochondria / Q000473:pathology; D008954:Models, Biological; D009206:Myocardium / Q000473:pathology; D009929:Organ Size; D010100:Oxygen / Q000737:chemistry; D012313:RNA / Q000737:chemistry; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
chemical_list: D012333:RNA, Messenger; D012313:RNA; C480024:COX5B protein, human; D003576:Electron Transport Complex IV; D010100:Oxygen