scholarly journals Biomechanical and neurohumoral stimulation of neonatal rat ventricular myocytes induce focal adhesion kinase phosphorylation at S910

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Miensheng Chu ◽  
Rekha Iyenar ◽  
Allen M Samarel
Keyword(s):  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Ventricular Myocytes ◽  
Neonatal Rat ◽  
Rat Ventricular Myocytes ◽  
Focal Adhesion Kinase Phosphorylation ◽  
Neonatal Rat Ventricular Myocytes ◽  
Kinase Phosphorylation ◽  
Stimulation Of

scholarly journals Heat stress activates AKT via focal adhesion kinase-mediated pathway in neonatal rat ventricular myocytes

2008 ◽  
Vol 295 (2) ◽  
pp. H561-H568 ◽  
Author(s):  
Hongguang Wei ◽  
Richard S. Vander Heide
Keyword(s):  
Heat Stress ◽  
Focal Adhesion Kinase ◽  
Signaling Pathways ◽  
Focal Adhesion ◽  
Ventricular Myocytes ◽  
Neonatal Rat ◽  
Wild Type ◽  
Rat Ventricular Myocytes ◽  
Myocardial Stress ◽  
Neonatal Rat Ventricular Myocytes

Heat stress (HS)-induced cardioprotection is associated with increased paxillin localization to the membrane fraction of neonatal rat ventricular myocytes (NRVM). The purpose of this study was 1) to examine the subcellular signaling pathways activated by HS; 2) to determine whether myocardial stress organizes and activates an integrated survival pathway; and 3) to investigate potential downstream cytoprotective proteins activated by HS. After HS, NRVM were subjected to chemical inhibitors (CI) designed to simulate ischemia by inhibiting both glycolysis and mitochondrial respiration. Protein kinase B (AKT) expression (wild type) was increased selectively with an adenoviral vector. Cell signaling was analyzed with Western blot analysis, while oncosis/apoptosis was assayed by measuring Trypan blue exclusion and/or terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling (TUNEL) staining, respectively. HS increased phosphorylation of focal adhesion kinase (FAK) at tyrosine 397 but did not adversely affect the viability of NRVM before CI. HS increased association between FAK and phosphatidylinositol 3-kinase as well as causing a significant increase in AKT activity. Increased expression of wild-type AKT protected myocytes from both oncotic and apoptotic cell death. Increased expression of a FAK inhibitor, FRNK, reduced AKT phosphorylation in response to HS both at time 0 and after 10 min of CI compared with myocytes expressing empty virus. We conclude that myocardial stress activates cytoskeleton-based signaling pathways that are associated with protection from lethal cell injury.

CARP Plays a Key Role in Cellular Growth Under Hypertrophic Stimuli in Neonatal Rat Ventricular Myocytes

2013 ◽  
Vol 9 ◽  
Author(s):  
Tara A Shrout
Keyword(s):  
Gene Expression ◽  
Ventricular Myocytes ◽  
Cellular Growth ◽  
Neonatal Rat ◽  
Transcriptional Level ◽  
Dual Nature ◽  
Hypertrophic Growth ◽  
Rat Ventricular Myocytes ◽  
Neonatal Rat Ventricular Myocytes ◽  
Over Time

Cardiac hypertrophy is a growth process that occurs in response to stress stimuli or injury, and leads to the induction of several pathways to alter gene expression. Under hypertrophic stimuli, sarcomeric structure is disrupted, both as a consequence of gene expression and local changes in sarcomeric proteins. Cardiac-restricted ankyrin repeat protein (CARP) is one such protein that function both in cardiac sarcomeres and at the transcriptional level. We postulate that due to this dual nature, CARP plays a key role in maintaining the cardiac sarcomere. GATA4 is another protein detected in cardiomyocytes as important in hypertrophy, as it is activated by hypertrophic stimuli, and directly binds to DNA to alter gene expression. Results of GATA4 activation over time were inconclusive; however, the role of CARP in mediating hypertrophic growth in cardiomyocytes was clearly demonstrated. In this study, Neonatal Rat Ventricular Myocytes were used as a model to detect changes over time in CARP and GATA4 under hypertrophic stimulation by phenylephrine and high serum media. Results were detected by analysis of immunoblotting. The specific role that CARP plays in mediating cellular growth under hypertrophic stimuli was studied through immunofluorescence, which demonstrated that cardiomyocyte growth with hypertrophic stimulation was significantly blunted when NRVMs were co-treated with CARP siRNA. These data suggest that CARP plays an important role in the hypertrophic response in cardiomyocytes.

scholarly journals Regulation of Ras·GTP Loading and Ras-Raf Association in Neonatal Rat Ventricular Myocytes by G Protein-coupled Receptor Agonists and Phorbol Ester

1999 ◽  
Vol 274 (28) ◽  
pp. 19762-19770 ◽  
Author(s):  
Antonio Chiloeches ◽  
Hugh F. Paterson ◽  
Richard Marais ◽  
Angela Clerk ◽  
Christopher J. Marshall ◽  
...  
Keyword(s):  
G Protein ◽  
Phorbol Ester ◽  
Ventricular Myocytes ◽  
Neonatal Rat ◽  
G Protein Coupled Receptor ◽  
Rat Ventricular Myocytes ◽  
Receptor Agonists ◽  
Neonatal Rat Ventricular Myocytes ◽  
G Protein Coupled
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