Alpha-1-adrenergic stimulation of phosphoinositide breakdown in cultured neonatal rat ventricular myocytes

1989 ◽  
pp. 73-75
Author(s):  
Johanna T. A. Meij ◽  
Jos M. J. Lamers
Keyword(s):  
Ventricular Myocytes ◽  
Neonatal Rat ◽  
Adrenergic Stimulation ◽  
Rat Ventricular Myocytes ◽  
Phosphoinositide Breakdown ◽  
Neonatal Rat Ventricular Myocytes ◽  
Stimulation Of

scholarly journals Gq- and ras-dependent pathways mediate hypertrophy of neonatal rat ventricular myocytes following alpha 1-adrenergic stimulation.

1994 ◽  
Vol 269 (18) ◽  
pp. 13490-13496 ◽  
Author(s):  
V.J. LaMorte ◽  
J. Thorburn ◽  
D. Absher ◽  
A. Spiegel ◽  
J.H. Brown ◽  
...  
Keyword(s):  
Ventricular Myocytes ◽  
Neonatal Rat ◽  
Adrenergic Stimulation ◽  
Rat Ventricular Myocytes ◽  
Neonatal Rat Ventricular Myocytes

scholarly journals Signaling responses after exposure to 5α-dihydrotestosterone or 17β-estradiol in norepinephrine-induced hypertrophy of neonatal rat ventricular myocytes

2010 ◽  
Vol 108 (3) ◽  
pp. 686-696 ◽  
Author(s):  
Yevgeniya E. Koshman ◽  
Mariann R. Piano ◽  
Brenda Russell ◽  
Dorie W. Schwertz
Keyword(s):  
Cell Size ◽  
Sex Hormones ◽  
Ventricular Myocytes ◽  
Neonatal Rat ◽  
Heart Cells ◽  
Adrenergic Stimulation ◽  
Rat Ventricular Myocytes ◽  
Extracellular Signal ◽  
17Β Estradiol ◽  
Neonatal Rat Ventricular Myocytes

Androgens appear to enhance, whereas estrogens mitigate, cardiac hypertrophy. However, signaling pathways in cells for short (3 min) and longer term (48 h) treatment with 17β-estradiol (E2) or 5α-dihydrotestosterone (DHT) are understudied. We compared the effect of adrenergic stimulation by norepinephrine (NE; 1 μM) alone or in combination with DHT (10 nM) or E2 (10 nM) treatment in neonatal rat ventricular myocytes (NRVMs) by cell area, protein synthesis, sarcomeric structure, gene expression, phosphorylation of extracellular signal-regulated (ERK), and focal adhesion kinases (FAK), and phospho-FAK nuclear localization. NE alone elicited the expected hypertrophy and strong sarcomeric organization, and DHT alone gave a similar but more modest response, whereas E2 did not alter cell size. Effects of NE dominated when used with either E2 or DHT with all combinations. Both sex hormones alone rapidly activated FAK but not ERK. Long-term or brief exposure to E2 attenuated NE-induced FAK phosphorylation, whereas DHT had no effect. Neither hormone altered NE-elicited ERK activation. Longer term exposure to E2 alone reduced FAK phosphorylation and reduced nuclear phospho-FAK, whereas its elevation was seen in the presence of NE with both sex hormones. The mitigating effects of E2 on the NE-elicited increase in cell size and the hypertrophic effect of DHT in NRVMs are in accordance with results observed in whole animal models. This is the first report of rapid, nongenomic sex hormone signaling via FAK activation and altered FAK trafficking to the nucleus in heart cells.

scholarly journals α-Adrenergic stimulation induces phosphorylation of retinoblastoma protein in neonatal rat ventricular myocytes

1997 ◽  
Vol 327 (1) ◽  
pp. 299-303 ◽  
Author(s):  
Qingquan LIU ◽  
Nicola J. DAWES ◽  
Yujuan LU ◽  
Huda S. SHUBEITA ◽  
Hong ZHU
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Myocytes ◽  
Ventricular Myocytes ◽  
Terminal Differentiation ◽  
Retinoblastoma Protein ◽  
Neonatal Rat ◽  
Adrenergic Stimulation ◽  
Hypertrophic Growth ◽  
Rat Ventricular Myocytes ◽  
Neonatal Rat Ventricular Myocytes

Mammalian cardiac myocytes become postmitotic shortly after birth, and the subsequent myocardial growth in adaptation to increasing workloads becomes primarily dependent on hypertrophy of existing myocytes. Although hypertrophic growth of cardiac myocytes has been extensively studied by using both in vitro and in vivo models, the molecular mechanism controlling the switch from hyperplastic to hypertrophic growth of cardiac myocytes is largely unknown. Since the majority of terminally differentiated cardiac myocytes are growth-arrested in G1/G0 phase, it has been hypothesized that the retinoblastoma protein (Rb) or its related pocket proteins which block G1/S transition becomes constitutively active during myocardial terminal differentiation. To test this hypothesis, we studied the regulation of Rb activity by α-adrenergic stimulation in neonatal rat ventricular myocytes which are mostly postmitotic in culture. Our results demonstrate that Rb is predominantly in the active hypophosphorylated state in control neonatal ventricular myocytes. α-Adrenergic stimulation activates G1/S transition in foetal but not neonatal rat ventricular myocytes. Although α-adrenergic stimulation does not activate G1/S transition in neonatal myocytes, it induces hyperphosphorylation of Rb to the same extent as in proliferating skeletal-muscle myoblasts or foetal ventricles. Hyper- but not hypo-phosphorylated Rb in stimulated neonatal myocytes or proliferating skeletal-muscle myoblasts fails to bind to the transcription factor, E2F, suggesting that hyperphosphorylated Rb is inactive. Therefore G1/S transition could also be blocked at steps in addition to Rb inactivation during terminal differentiation and these blockades are refractory to α-adrenergic stimulation.

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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