Increasing Transforming Growth Factor Beta-1 and its Receptor Expression in Human Myocardium with End-Stage Congestive Heart Failure.

2000 ◽  
Vol 6 (S2) ◽  
pp. 612-613
Author(s):  
S. Ren ◽  
C. Wei
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Normal Subjects ◽  
Human Myocardium ◽  
Receptor Expression ◽  
Growth Factor Beta ◽  
End Stage

Transforming growth factor-beta (TGF-β) is a growth-regulating peptide that has been shown to enhance collagen production both in vivo and in vitro. The previous studies demonstrated that TGF-β 1 is present in the normal animal myocardium. However, the expression and localization of TGF-β 1 and TGF-P receptor in human myocardium remain unclear. Therefore, the present study was designed to determine the TGF-β 1 and its receptor in human myocardium in normal subjects and in patients with end-stage congestive heart failure (CHF).Human ventricular tissues were obtained from five normal subjects and five patients with end-stage CHF during cardiac transplantation. TGF-β 1 and TGF-beta type I receptor (TGF-βRI) were determined by immunohistochemical staining (IHCS). The results of IHCS was evaluated by staining density scores (0, no staining; 1, minimal staining; 2, mild staining; 3, moderate staining; and 4, strong staining). The positive staining area (+%) in entire section was also determined.

Presence of P53 and Transforming Growth Factor Beta-1 in Human Cardiac Tissue With Congestive Heart Failure

1997 ◽  
Vol 3 (S2) ◽  
pp. 149-150
Author(s):  
Hong Song ◽  
Ren Shuxun ◽  
Xia Fen ◽  
Zhang Ruiwen ◽  
Wei Chi-Ming
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Normal Subjects ◽  
Ventricular Myocardium ◽  
Growth Factor Beta ◽  
Human Ventricular Myocardium ◽  
Tgf Β1

p53 is a tumor suppressor gene which involves apoptosis and cell cycle arrest under certain stress stimulate. The expression of p53 is associated with ischemia-reperfussion induced myocardial apoptosis in rat and with the development of coronary artery restenosis after angioplasty in humans. However, the status of p53 in human cardiomyocytes and fibroblasts in congestive heart failure (CHF) remains controversial.Transforming growth factor-beta (TGF-β) is a growth-regulating peptide that has been shown to enhance collagen production both in vivo and in vitro in cultured cells. Both p53 and TGF-β may inhibit the cell growth and induce cellular apoptosis. While the previous studies demonstrated that TGF-β1 is present in the animal myocardium, the presentation and localization of TGF-β1 in human myocardium remain unclear.Therefore, the present study was designed to investigate the p53 and TGF-β1 in human ventricular myocardium in normal subjects and in patients with heart failure. Five normal subjects and five end-stage failing human ventricular myocardium tissue were obtained from cardiac transplantation.

Transforming growth factor beta 1 (TGF-beta 1) in atrial fibrillation and acute congestive heart failure

2010 ◽  
Vol 100 (4) ◽  
pp. 335-342 ◽  
Author(s):  
Michael Behnes ◽  
Ursula Hoffmann ◽  
Siegfried Lang ◽  
Christel Weiss ◽  
Parviz Ahmad-Nejad ◽  
...  
Keyword(s):  
Heart Failure ◽  
Atrial Fibrillation ◽  
Congestive Heart Failure ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Tgf Beta ◽  
Growth Factor Beta

Decrease Tyrosine Phosphorylation of Stat3 in Human Myocardium with End-Stage Congestive Heart Failure

2000 ◽  
Vol 6 (S2) ◽  
pp. 596-597
Author(s):  
C. Wei ◽  
J. S. McLaughlin
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Protein Expression ◽  
Cardiac Tissue ◽  
Normal Subjects ◽  
Human Myocardium ◽  
Stat3 Phosphorylation ◽  
Normal Human ◽  
Human Cardiac Tissue ◽  
End Stage

Recent study demonstrated that decrease signal transducer and activator of transcription-3 (STAT3) phosphorylation and increase apoptosis might be a critical point in the transition between compensatory cardiac hypertrophy and heart failure. To date, the protein expression of STAT3 in normal and failing human heart remains unclear. Therefore, the current study was designed to investigate the protein expression of STAT3 in human myocardium with end-stage congestive heart failure (CHF) and compared with that in normal human cardiac tissue.Human cardiac atrial tissue was obtained from normal subjects (n=5) and end-stage CHF patients (n=5) during cardiac transplantation. To detect the DNA fragmentation, in situ terminal deoxymucleotidyl transferase dUTP nick end labeling (TUNEL) was performed. An average of 1000 nuclei was analyzed for TUNEL study. STAT3 protein expression and phosphorylation of STAT3 were determined by immunohistochemical staining (IHCS) with total STAT3 and phospho-specific STAT3 antibodies.

9 Ivabradine Alters Fibroblast Number and Transforming Growth Factor beta 1 Expression in Heart Failure

Heart ◽  
2014 ◽  
Vol 100 (Suppl 1) ◽  
pp. A4.2-A4
Author(s):  
P Dias ◽  
M Navaratnarajah ◽  
S Alayoubi ◽  
J E Cartledge ◽  
N Jayaratne ◽  
...  
Keyword(s):  
Heart Failure ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Growth Factor Beta

scholarly journals Role of bradykinin B2 receptors in neonatal kidney growth.

1997 ◽  
Vol 8 (6) ◽  
pp. 920-928
Author(s):  
I V Yosipiv ◽  
S Dipp ◽  
S S el-Dahr
Keyword(s):  
Body Weight ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Receptor Expression ◽  
Kidney Growth ◽  
Growth Factor Beta ◽  
Hoe 140 ◽  
Neonatal Kidney

The kallikrein-kinin system is developmentally expressed in newborn kidneys. In addition, bradykinin (BK) is mitogenic in cultured glomerular mesangial cells. However, the role of endogenous BK in postnatal renal development has not been defined. In this study, the role of the BK-B2 receptor in neonatal kidney growth in the rat was examined. RNA blot analysis and semiquantitative reverse transcription-polymerase chain reaction showed that BK-B2 mRNA levels were approximately 30- to 40-fold higher in newborn than adult kidneys. Treatment of newborn rats with the selective BK-B2 antagonist, Hoe 140 (600 micrograms/kg per day, sc), from days 1 through 14 of life significantly reduced body weight, kidney-to-body weight ratios, and kidney DNA content, compared with saline-treated controls. Hoe 140 treatment had no effect on kidney protein or RNA content or the expression of transforming growth factor-beta mRNA. The growth retardation induced by BK-B2 blockade was observed only in the kidney and, to a lesser extent, in the heart. BK-B2 blockade had no effect on renal growth in adult rats, suggesting that these effects are developmentally regulated. In contrast to Hoe 140 treatment, neonatal protein undernutrition resulted in a generalized reduction in kidney DNA, RNA, and protein contents; increased renal transforming growth factor-beta gene expression; and decreased renal kallikrein expression and enzymatic activity. The results suggest that activation of BK-B2 receptor expression in the neonatal kidney plays an important role in the regulation of DNA synthesis during the latter stages of nephrogenesis.

Sign in / Sign up

Export Citation Format

Share Document