Consulta: subjectFacets:"Myocardial hypertrophy"
Registros recuperados: 5
Data/hora: 06/06/2024 01:02:19

Immediate response of myocardium to pressure overload includes transient regulation of genes associated with mitochondrial bioenergetics and calcium availability
Provedor de dados: 74
Autores: Deckmann,Ana Carolina; Theizen,Thaís Holz; Medrano,Francisco Javier; Franchini,Kleber Gomes; Pereira,Gonçalo Amarante Guimarães.
Ventricular hypertrophy is one of the major myocardial responses to pressure overload (PO). Most studies on early myocardial response focus on the days or even weeks after induction of hypertrophic stimuli. Since mechanotransduction pathways are immediately activated in hearts undergoing increased work load, it is reasonable to infer that the myocardial gene program may be regulated in the first few hours. In the present study, we monitored the expression of some genes previously described in the context of myocardial hypertrophic growth by using the Northern blot technique, to estimate the mRNA content of selected genes in rat myocardium for the periods 1, 3, 6, 12 and 48 h after PO stimuli. Results revealed an immediate switch in the expression of genes...
Tipo: Info:eu-repo/semantics/article
Palavras-chave: Pressure overload; Myocardial hypertrophy; Gene expression; SERCA2.
Ano: 2010
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572010000100004

BMP4 Induces Cardiomyocyte Hypertrophy Through the Activation of ERK 1/2 Signaling Pathway in H9c2 Cells
Provedor de dados: 52
Autores: Yuan,Yu; Tao,Yezheng; Deng,Yongzhi; Ye,Qunhui; Lin,Bin; Wu,Lin.
Abstract Bone morphogenetic protein-4 (BMP4) is a member of the bone morphogenetic protein family which plays an important role in bone formation, inflammation and cardiac hypertrophy. The aim of this study was to investigate the underlying molecular mechanism that BMP4-induced cardiomyocyte hypertrophy. H9c2 cells were used to measure cell surface area and protein synthesis. Western blot was used to examine hypertrophic marker brain natriuretic peptide (BNP) protein expression and phosphorylation of ERK1/2. The results exhibited that cell surface area, protein synthesis and BNP protein expression were increased with BMP4 treatment. While PD98059 inhibited these effects of BMP4. In addition, BMP4 treatment increased phosphorylation of ERK1/2 in a time- and...
Tipo: Info:eu-repo/semantics/article
Palavras-chave: BMP4; Myocardial hypertrophy; ERK1/2 signaling pathway.
Ano: 2019
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1516-89132019000100315

The role of Ca2+/calmodulin-dependent protein kinase II and calcineurin in TNF-α-induced myocardial hypertrophy
Provedor de dados: 56
Autores: Wang,Gui-Jun; Wang,Hong-Xin; Yao,Yu-Sheng; Guo,Lian-Yi; Liu,Pei.
We investigated whether Ca2+/calmodulin-dependent kinase II (CaMKII) and calcineurin (CaN) are involved in myocardial hypertrophy induced by tumor necrosis factor α (TNF-α). The cardiomyocytes of neonatal Wistar rats (1-2 days old) were cultured and stimulated by TNF-α (100 μg/L), and Ca2+ signal transduction was blocked by several antagonists, including BAPTA (4 µM), KN-93 (0.2 µM) and cyclosporin A (CsA, 0.2 µM). Protein content, protein synthesis, cardiomyocyte volumes, [Ca2+]i transients, CaMKIIδB and CaN were evaluated by the Lowry method, [³H]-leucine incorporation, a computerized image analysis system, a Till imaging system, and Western blot analysis, respectively. TNF-α induced a significant increase in protein content in a dose-dependent manner...
Tipo: Info:eu-repo/semantics/article
Palavras-chave: Myocardial hypertrophy; Tumor necrosis factor α; Calcium; Calmodulin-dependent kinase; Calcineurin.
Ano: 2012
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2012001100008

Etanercept protects rat cardiomyocytes against hypertrophy by regulating inflammatory cytokines secretion and cell apoptosis
Provedor de dados: 56
Autores: Li,Q.; Yu,Q.; Na,R.; Liu,B.
We aimed to investigate the effect of etanercept, a tumor necrosis factor-α (TNF-α) inhibitor, on rat cardiomyocyte hypertrophy and its underlying mechanism. Primary neonatal rat cardiomyocytes were isolated from Sprague-Dawley rats. The model of rat cardiomyocyte hypertrophy was induced by endothelin, and then treated with different concentrations of etanercept (1, 10, and 50 μM). After treatment, cell counts, viability and cell apoptosis were evaluated. The mRNA levels of myocardial hypertrophy marker genes, including atrial natriuretic factor (ANF), matrix metalloproteinase (MMP)-9 and MMP-13, were detected by qRT-PCR, and the expressions of apoptosis-related proteins (Bcl-2 and Bax) were measured by western blotting. The protein levels of transforming...
Tipo: Info:eu-repo/semantics/article
Palavras-chave: Tumor necrosis factor-α inhibitor; Endothelin; Myocardial hypertrophy; Cell apoptosis; Inflammatory response.
Ano: 2017
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2017000600604

Myocardial contractility of the isovolumetrically beating isolated rat heart
Provedor de dados: 56
Autores: De Stefano,L.M.; Matsubara,L.S.; Matsubara,B.B.
Several indexes of myocardial contractility have been proposed to assess ventricular function in the isovolumetrically beating isolated heart. However, the conclusions reached on the basis of these indexes may be influenced by ventricular geometry rather than contractility itself. The objective of the present study was to assess the performance of widely used contractility indexes in the isovolumetrically beating isolated heart in two experimental models of hypertrophy, the spontaneously hypertensive rat (SHR) and infrarenal aortocava fistula. Compared to normotensive controls (N = 8), SHRs with concentric hypertrophy (N = 10) presented increased maximum rate of ventricular pressure rise (3875 ± 526 vs 2555 ± 359 mmHg/s, P &lt; 0.05) and peak of...
Tipo: Info:eu-repo/semantics/article
Palavras-chave: Myocardial hypertrophy; Ventricular dilation; Pressure overload; Volume overload.
Ano: 2004
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2004001000017