Angiotensin II stimulates hypertrophic growth of cultured neonatal rat ventricular myocytes: roles of PCK and PGF2alpha

2000 ◽  
Vol 62 (4) ◽  
pp. 233-237 ◽  
Author(s):  
G.K Oriji
Keyword(s):  
Angiotensin Ii ◽  
Ventricular Myocytes ◽  
Neonatal Rat ◽  
Hypertrophic Growth ◽  
Rat Ventricular Myocytes ◽  
Neonatal Rat Ventricular Myocytes

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 Suppressor of Cytokine Signaling 3 Is Induced by Angiotensin II in Heart and Isolated Cardiomyocytes, and Participates in Desensitization

Endocrinology ◽  
2003 ◽  
Vol 144 (10) ◽  
pp. 4586-4596 ◽  
Author(s):  
Vivian C. Calegari ◽  
Rosangela M. N. Bezerra ◽  
Márcio A. Torsoni ◽  
Adriana S. Torsoni ◽  
Kleber G. Franchini ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Rat Heart ◽  
Ventricular Myocytes ◽  
Janus Kinase ◽  
Neonatal Rat ◽  
Cytokine Signaling ◽  
Ang Ii ◽  
Suppressor Of Cytokine Signaling ◽  
Rat Ventricular Myocytes ◽  
Neonatal Rat Ventricular Myocytes

Angiotensin II (Ang II) exerts a potent growth stimulus on the heart and vascular wall. Activation of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) intracellular signaling pathway by Ang II mediates at least some of the mitogenic responses to this hormone. In other signaling systems that use the JAK/STAT pathway, proteins of the suppressor of cytokine signaling (SOCS) family participate in signal regulation. In the present study it is demonstrated that SOCS3 is constitutively expressed at a low level in rat heart and neonatal rat ventricular myocytes. Ang II at a physiological concentration enhances the expression of SOCS3 mRNA and protein, mainly via AT1 receptors. After induction, SOCS3 associates with JAK2 and impairs further activation of the JAK2/STAT1 pathway. Pretreatment of rats with a specific phosphorthioate antisense oligonucleotide to SOCS3, reverses the desensitization to angiotensin signaling, as detected by a fall in c-Jun expression after repetitive infusions of the hormone. Thus, SOCS3 is induced by Ang II in rat heart and neonatal rat ventricular myocytes and participates in the modulation of the signal generated by this hormone.

scholarly journals Prostaglandin F2αStimulates Hypertrophic Growth of Cultured Neonatal Rat Ventricular Myocytes

1996 ◽  
Vol 271 (2) ◽  
pp. 1179-1186 ◽  
Author(s):  
John W. Adams ◽  
Darren S. Migita ◽  
Maggie K. Yu ◽  
Robert Young ◽  
Mark S. Hellickson ◽  
...  
Keyword(s):  
Ventricular Myocytes ◽  
Neonatal Rat ◽  
Hypertrophic Growth ◽  
Rat Ventricular Myocytes ◽  
Neonatal Rat Ventricular Myocytes

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.

Effect of Intermedin1-53 on Angiotensin II-Induced Hypertrophy in Neonatal Rat Ventricular Myocytes

2010 ◽  
Vol 56 (1) ◽  
pp. 45-52 ◽  
Author(s):  
Jing-Hui Yang ◽  
Cun-Gen Ma ◽  
Yan Cai ◽  
Chun-Shui Pan ◽  
Jing Zhao ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Ventricular Myocytes ◽  
Neonatal Rat ◽  
Rat Ventricular Myocytes ◽  
Neonatal Rat Ventricular Myocytes
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