Intracardiac basic fibroblast growth factor and transforming growth factor-beta 1 mRNA and their proteins expression level in patients with pressure or volume-overload right or left ventricular hypertrophy.
OBJECTIVE
The aim of the study was to investigate the pathogenic role of intracardiac basic fibroblast growth factor (bFGF) and transforming growth factor beta-1 (TGF beta-1) mRNA and their protein expression level in patients with ventricular volume or pressure-overload.


BACKGROUND
Myocardial hypertrophy is responsiveness of cardiomyocytes and interstitial cells to ventricular stress produced by ventricular preload or/and afterload and a series of growth factors. However, the molecular mechanism by which the changes of bFGF and TGF beta-1 mRNA and their protein expression level in patients with volume or pressure-overload lead to distinct forms of cardiac hypertrophy is unclear.


METHODS
32 patients were divided into two groups: 16 patients with cardiac volume overload leading to left ventricular hypertrophy (VG) and 16 patients with pressure overload leading to right ventricular hypertrophy (PG), respectively, as compared with 5 unexpected deaths of noncardiac disease (CG), which is determinated by echocardiography and/or pathologic examination following operation; intracardiac bFGF and TGF beta-1 mRNA and their protein expression level were determined by immunohistochemistry and in situ hybridization as well as image analysis; cardiomyocytes and fibril collagen of type I and III were examined by haemotoxylin and eosin (HE) staining or sirius-red staining.


RESULTS
Cardiocyte transverse diameter and fibril collagen of extracellular matrix, intracardiac bFGF and TGF beta-1 mRNA and their protein expression level in patients with volume or pressure-overload were significantly increased in both VG and PG, as compared with CG.


CONCLUSIONS
This is the first paper to suggest that intracardiac bFGF and TGF beta-1 play a pivotal role in patients with pressure or volume-overload leading to right or left ventricular hypertrophy, composed of cardiomyocyte hypertrophy and extracellular matrix proliferation.
He
Zuo Yun
ZY
Department of Cardiology, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China. yslhzy@yahoo.com.cn
Feng
Bing
B
Yang
Sheng Li
SL
Luo
Hui Lan
HL
D000293:Adolescent; D000328:Adult; D015415:Biomarkers / Q000032:analysis; D001707:Biopsy, Needle; D001774:Blood Chemical Analysis; D002648:Child; D015331:Cohort Studies; D015150:Echocardiography, Doppler; D005260:Female; D016222:Fibroblast Growth Factor 2 / Q000032:analysis / Q000378:metabolism*; D006334:Heart Function Tests; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000378:metabolism* / Q000503:physiopathology*; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D008297:Male; D011379:Prognosis; D012333:RNA, Messenger / Q000032:analysis; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D016212:Transforming Growth Factor beta / Q000032:analysis / Q000378:metabolism*; D053773:Transforming Growth Factor beta1; D017725:Ventricular Pressure / Q000502:physiology*
D015415:Biomarkers; D012333:RNA, Messenger; C508960:TGFB1 protein, human; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; D016222:Fibroblast Growth Factor 2