The profile of cardiac cytochrome c oxidase (COX) expression in an accelerated cardiac-hypertrophy model.
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.
Kuo
Wei-Wen
WW
Institute of Biochemistry, Chung-Shan Medical University, Taichung, Taiwan, ROC.
Chu
Chia-Yih
CY
Wu
Chieh-Hsi
CH
Lin
James A
JA
Liu
Jer-Yuh
JY
Ying
Tsung-Ho
TH
Lee
Shin-Da
SD
Hsieh
Yi-Hsien
YH
Chu
Chu-Hsien
CH
Lin
Ding-Yu
DY
Hsu
Hsi-Hsien
HH
Huang
Chih-Yang
CY
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
D012333:RNA, Messenger; D012313:RNA; C480024:COX5B protein, human; D003576:Electron Transport Complex IV; D010100:Oxygen