[Differential expression of cardiac immediate early and late response gene in exercise-induced and hypertensive cardiac hypertrophic remodeling].
Our previous studies have shown that the myocardial phenotypes between exercise-induced and hypertensive cardiac hypertrophy are different. However, alteration of cardiac gene expression in the two kinds of hypertrophy is not clear. We therefore studied the expression of immediate early and late responsive gene in Wistar rats subject to a 12-weeks swimming program and spontaneously hypertensive rats (SHR) by Northern blot. The autoradiographs were analyzed by scanning densitometry. When compared with matched sedentary control, swimming rats and SHR increased their heart/body weight by 29% and 61% respectively (P < 0.01). After a series of swimming program, levels of c-fos and atrial natriuretic factor (ANF) mRNA were instantly increased 203% and 214% respectively in the swimming rats. However in 24 h after swimming, ANF mRNA was decreased to the level of control but c-fos mRNA was still higher than than in control. The levels of c-fos and ANF mRNA were increased by 80% and 298% in SHR respectively. The expression of beta-myosin heavy chain (MHC) mRNA was increased by 117% in SHR but decreased by 12% in swimming rats. The expression of alpha-MHC mRNA was decreased by 42% in SHR but unchanged in swimming rats. The abundance alpha/beta-MHC mRNA in swimming rats is 336% higher than in SHR. These results showed differential expression of the immediate early and late responsive gene in exercise-induced and SHR hypertrophied heart remodeling. It is suggested that (1) the differential expression of c-fos gene may differently regulate remodeling of these two cardiac hypertrophies; (2) the differential expression of ANF gene may be a molecular marker for distinguishing the two kinds of cardiac hypertrophy; and (3) the differential expression of alpha/beta-MHC gene ratio may regulate exercise-induced and hypertensive hypertrophied myocardial cell changing to contractile phenotype and synthetic phenotype respectively, at the gene transcription level.
Li
Z B
ZB
Institute of Sports Medicine, Beijing Medical University, Beijing 100083.
Gao
Y Q
YQ
Tang
Z S
ZS
D000818:Animals; D006332:Cardiomegaly / Q000209:etiology / Q000235:genetics*; D006973:Hypertension / Q000150:complications / Q000235:genetics*; D008297:Male; D020409:Molecular Motor Proteins; D009206:Myocardium / Q000378:metabolism*; D018995:Myosin Heavy Chains / Q000096:biosynthesis* / Q000235:genetics; D024501:Nonmuscle Myosin Type IIB; D010641:Phenotype; D005082:Physical Exertion; D016760:Proto-Oncogene Proteins c-fos / Q000096:biosynthesis* / Q000235:genetics; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D017208:Rats, Wistar; D014158:Transcription, Genetic
D020409:Molecular Motor Proteins; C491238:Myh9 protein, rat; D016760:Proto-Oncogene Proteins c-fos; D012333:RNA, Messenger; D024501:Nonmuscle Myosin Type IIB; C103815:nonmuscle myosin type IIB heavy chain; D018995:Myosin Heavy Chains