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.

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.

Enhancement of Endothelin Converting Enzyme and Endothelin Receptor Subtypes in Human Myocardium with Congestive Heart Failure

2000 ◽  
Vol 6 (S2) ◽  
pp. 608-609
Author(s):  
J. Lin ◽  
C Wei
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Cardiac Tissue ◽  
Vascular Endothelial Cells ◽  
Normal Subjects ◽  
Human Myocardium ◽  
Endothelin Receptors ◽  
Receptor Subtypes ◽  
Converting Enzyme ◽  
Endothelin Converting Enzyme

Endothelin-1 (ET-1) is a potent endothelial cell-drived vasoconstrictive peptide which is increased in congestive heart failure (CHF). ET-1 is converted from its precursor big ET-1 by activation of endothelin converting enzyme (ECE). ET-1 binding to ET-A receptor in vascular smooth muscle cells stimulates vasoconstriction and binding to ET-B receptor in vascular endothelial cells mediates vasodilation. In previous studies, we and others demonstrated that plasma ET-1 was significantly increased in congestive heart failure. However, the presentation and localization of endothelin converting enzyme and endothelin receptors (ET-A and ET-B) in human cardiac tissue with and without heart failure remain unclear. Therefore, the current study was designed to investigate the expression and localization of endothelin receptors and endothelin converting enzyme in human myocardium in the absence or presence of congestive heart failure.Human atrial tissues (n=6) were obtained from normal subjects and end-stage CHF patients during cardiac transplantation. The expression of ECE, ET-A and ET-B were determined by immunohistochemical staining (IHCS).

Expression of Angiotensin II Type 1 and Type 2 Receptor in Human Myocardium with Congestive Heart Failure

2000 ◽  
Vol 6 (S2) ◽  
pp. 618-619
Author(s):  
P. Y. Lau ◽  
M. G. Cardarelli ◽  
C. Wei
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Angiotensin Ii ◽  
Cardiac Tissue ◽  
Open Heart Surgery ◽  
Human Myocardium ◽  
Receptor Expression ◽  
At2 Receptors

Angiotensin II (AH) is a potent vasoconstrictor and mitogenic factor. AH receptors include type 1 (ATI) and type 2 (AT2) receptors. Recent studies demonstrated that both ATI and AT2 receptors expressed in human myocardium. Circulating and local tissue level of AH was increased in severe congestive heart failure (CHF). However, the expression of ATI and AT2 in cardiac tissue with CHF remains controversial. Therefore, the present study was designed to investigate the protein expression of ATI and AT2 receptors in normal human myocardium and in human cardiac tissue with mild and severe CHF.Human atrial tissues from normal subjects and CHF patients with ischemic cardiomyopathy and dilated cardiomyopathy were obtained from open-heart surgery and cardiac transplantation. ATI and AT2 receptor expression was investigated by immunohistochemical staining (IHCS). The results of IHCS was evaluated by IHCS staining density scores (0, no staining; 1, minimal staining; 2, mild staining; 3, moderate staining; and 4, strong staining).

Increasing Apoptosis-Related Gene Expression in Human Myocardium with Congestive Heart Failure

2000 ◽  
Vol 6 (S2) ◽  
pp. 628-629
Author(s):  
D. Xie ◽  
C. Wei
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Normal Subjects ◽  
Left Ventricular ◽  
Cardiac Tissues ◽  
Human Cardiomyocytes ◽  
Cycle Arrest ◽  
Induced Apoptosis ◽  
End Stage ◽  
Apoptosis Related Gene

Regulation of apoptosis involves a number of genes that can be classified into broad categories. These include genes that act as effectors of apoptosis, such as p53, c-myc, bax, p21- WAF, and genes that primarily suppress apoptosis, such as Bcl-2 gene family. These genes have been reported to be responsible for the modulation of certain stress induced apoptosis and cell cycle arrest.It has also been reported that apoptosis involved in cardiovascular diseases such as myocardial infarction, reperfusion injury, left ventricular hypertrophy, and hypertension. However, the expression of apoptosis-related genes in human cardiomyocytes in normal subjects and in patients with congestive heart failure (CHF) remains unclear. Therefore, the present study was designed to determine the expression and localization of apoptosis-related genes in human heart.Five normal subjects and five end-stage CHF human ventricular cardiac tissues were obtained from cardiac transplantation. The expression of p53, p21-WAF and Bcl-2 were determined by immunohistochemical staining (IHCS).

scholarly journals Gene expression of adrenomedullin in failing myocardium: comparison to atrial natriuretic peptide

2002 ◽  
Vol 92 (3) ◽  
pp. 1058-1063 ◽  
Author(s):  
Anselm T. Bäumer ◽  
Christina Schumann ◽  
Bodo Cremers ◽  
Gabi Itter ◽  
Wolfgang Linz ◽  
...  
Keyword(s):  
Heart Failure ◽  
Dilated Cardiomyopathy ◽  
Normal Subjects ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Human Myocardium ◽  
Idiopathic Dilated Cardiomyopathy ◽  
Left Ventricular Myocardium ◽  
End Stage ◽  
Atrial Natriuretic

The expression of adrenomedullin (AM) and atrial natriuretic factor (ANF) were investigated in the myocardium of a rat model of chronic ischemic heart failure (CHF) compared with sham-operated controls. In addition, human myocardium of patients with end-stage heart failure due to idiopathic dilated cardiomyopathy compared with myocardium of normal subjects (NF) was studied. In CHF, similar AM levels but increased ANF expression were observed in left ventricular myocardium, as assessed by semiquantitative PCR. Functional experiments with freshly excised papillary muscles showed no influence of AM on myocardial contractility. In NF human myocardium, the expression of AM mRNA was threefold higher in atrial compared with ventricular tissue. In analogy, ANF mRNA was increased by ∼15-fold in atrial tissue. In dilated cardiomyopathy, the expression of AM was significantly increased in right and left ventricles compared with NF. In parallel, ventricular ANF expression was enhanced.

Increased DNA Damage and Decreased H-MYH Protein Expression in Human Myocardium with End-Stage Congestive Heart Failure

2001 ◽  
Vol 7 (S2) ◽  
pp. 72-73
Author(s):  
R. Lin ◽  
Y. Dong ◽  
J.V. Conte ◽  
A-L Lu-Chang ◽  
C. Wei
Keyword(s):  
Heart Failure ◽  
Dna Damage ◽  
Congestive Heart Failure ◽  
Oxidative Damage ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Dna Lesions ◽  
Human Myocardium ◽  
End Stage

The reactive oxygen species (ROS) such as superoxide radical (O2), hydrogen peroxide (H2O2), and hydroxyl radical (OH), plays a critical role in the pathogenesis of hypertension, atherosclerosis, ischemia-reperfusion injury, stroke, myocardial infarction, and congestive heart failure. A recent study demonstrated that the frequency of mutation in a reporter gene increased in cortical DNA after forebrain ischemia-reperfusion. Eight DNA lesions that are characteristic of DNA damage mediated by free radicals were detected. Among the different oxidative-damage DNA products, 8-oXo-7,8-dihydrodeoxyguanine (8-oxoG) is the most stable and deleterious adduct. Recent studies demonstrated that human MutY homologue (hMYH) protein plays important role in repairing oxidative damage. to date, there is no information regarding the role of hMYH expression in human myocardium with congestive heart failure (CHF). Therefore, the current study designed to investigate the levels of hMYH expression and 8-oxoG in myocardium in the absence or presence of end-stage congestive heart failure. The hypothesis of this study is that increasing DNA damage such as 8-oxoG generation is associated with a reduction of hMYH expression in human myocardium with congestive heart failure.

Neutrophil-activating peptide-2 in patients with pulmonary edema from congestive heart failure or ARDS

1993 ◽  
Vol 264 (5) ◽  
pp. L490-L495 ◽  
Author(s):  
A. B. Cohen ◽  
M. D. Stevens ◽  
E. J. Miller ◽  
M. A. Atkinson ◽  
G. Mullenbach ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
High Performance Liquid Chromatography ◽  
Liquid Chromatography ◽  
Pulmonary Edema ◽  
High Performance ◽  
Distress Syndrome ◽  
Normal Subjects ◽  
Antigen Concentration ◽  
Fluid Formation

We carried out studies to determine whether the neutrophil-activation peptide-2 (NAP-2) plays a role in the recruitment and/or degranulation of neutrophils into the lungs of patients with the adult respiratory distress syndrome (ARDS) or congestive heart failure (CHF). NAP-2 precursors plus NAP-2 (beta-thromboglobulin-like antigen) were measured in lung fluids and plasmas with a radioimmunoassay, and NAP-2 was separated from its precursors by high-performance liquid chromatography. Pulmonary edema fluids (PEFs) from patients with CHF contained higher concentrations of the beta-thromboglobulin-like antigen than PEFs from patients with ARDS, and bronchoalveolar lavage fluids (BALs) from patients with ARDS contained higher concentrations of beta-thromboglobulin-like antigen than BALs from normal subjects. beta-Thromboglobulin-like antigen concentration was 4.1-fold greater in PEFs from patients with CHF than in their plasmas. Chemotactically active NAP-2 was also demonstrated in PEFs but not in plasmas from patients with CHF and ARDS. These data suggest that significant platelet degranulation occurred into the lungs of the patients with CHF and that NAP-2 and other platelet constituents may contribute to fluid formation in patients with CHF.

scholarly journals Survival advantage of hemodialysis relative to peritoneal dialysis in patients with end-stage renal disease and congestive heart failure

2011 ◽  
Vol 80 (9) ◽  
pp. 970-977 ◽  
Author(s):  
Florence Sens ◽  
Anne-Marie Schott-Pethelaz ◽  
Michel Labeeuw ◽  
Cyrille Colin ◽  
Emmanuel Villar
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Peritoneal Dialysis ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
Survival Advantage ◽  
Stage Renal Disease ◽  
End Stage
Sign in / Sign up

Export Citation Format

Share Document