|
|
|
|
| |
|
|
| 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 |
| |
|
|
| 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 |
| |
|
| |
|
|
| 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 |
| |
|
|
|
