Collaborative Roles For C-Jun N-Terminal Kinase, C-Jun, Serum Response Factor, And Sp1 In Calcium-Regulated Myocardial Gene Expression, Patrick M. Mcdonough, Deanna S. Hanford, Amy B. Sprenkle, Noel R. Mellon, Christopher C. Glembotski
Sep 1997
Collaborative Roles For C-Jun N-Terminal Kinase, C-Jun, Serum Response Factor, And Sp1 In Calcium-Regulated Myocardial Gene Expression, Patrick M. Mcdonough, Deanna S. Hanford, Amy B. Sprenkle, Noel R. Mellon, Christopher C. Glembotski
Amy Sprenkle
Electrical stimulation of contractions (pacing) of primary neonatal rat ventricular myocytes increases intracellular calcium and activates a hypertrophic growth program that includes expression of the cardiac-specific gene, atrial natriuretic factor (ANF). To investigate the mechanism whereby pacing increases ANF, pacing was tested for its ability to regulate mitogen-activated protein kinase family members, ANF promoter activity, and the trans-activation domain of the transcription factor, Sp1. Pacing and the calcium channel agonist BAYK 8644 activated c-Jun N-terminal kinase (JNK) but not extracellular signal-regulated kinase. Pacing stimulated ANF-promoter activity approximately 10-fold. Furthermore, transfection with an expression vector for c-Jun, a substrate for JNK, …
Myocardial Alpha-Thrombin Receptor Activation Induces Hypertrophy And Increases Atrial Natriuretic Factor Gene Expression, C C. Glembotski, C E. Irons, K A. Krown, S F. Murray, A B. Sprenkle, C A. Sei
Sep 1993
Myocardial Alpha-Thrombin Receptor Activation Induces Hypertrophy And Increases Atrial Natriuretic Factor Gene Expression, C C. Glembotski, C E. Irons, K A. Krown, S F. Murray, A B. Sprenkle, C A. Sei
Amy Sprenkle
The protease, a-thrombin (aTh), affects myocardial cell contractility, a feature common among agents that induce hypertrophy. However, it is not known whether cardiac myocytes possess aTh receptors (aTh-R), or if long term treatment with aTh can enhance growth and gene expression. In the present study primary neonatal rat ventricular myocytes expressed a 3.6-kilobase mRNA species that hybridized with a rat aTh-R-specific probe. After 48 h, aTh induced hypertrophy, sarcomeric organization, and enhanced atrial natriuretic factor (ANF) expression, all of which were blocked by the aTh-selective protease inhibitor, D-Phe-Pro-Argchloromethyl ketone. The aTh-R agonist peptide, SFLLRNPND, was a potent activator of ANF …
The Alpha-Adrenergic Stimulation Of Atrial Natriuretic Factor Expression In Cardiac Myocytes Requires Calcium Influx, Protein Kinase C, And Calmodulin-Regulated Pathways, C A. Sei, C E. Irons, A B. Sprenkle, P M. Mcdonough, J H. Brown, C C. Glembotski
Aug 1991
The Alpha-Adrenergic Stimulation Of Atrial Natriuretic Factor Expression In Cardiac Myocytes Requires Calcium Influx, Protein Kinase C, And Calmodulin-Regulated Pathways, C A. Sei, C E. Irons, A B. Sprenkle, P M. Mcdonough, J H. Brown, C C. Glembotski
Amy Sprenkle
It has been shown recently that a-adrenergic agonists can stimulate atrial natriuretic factor (ANF) expression in ventricular cardiac myocytes; however, little is known about the intracellular signals mediating this activation. The present study focused on the potential roles of calcium-regulated kinases and calcium influx in the a-adrenergic stimulation of ANF gene expression in ventricular myocardial cell cultures. Myocardial cells maintained for 48 h in serumfree medium supplemented with phenylephrine (PE) possessed up to 15-fold higher levels of ANF peptide and ANF mRNA than control cells. The removal of PE, or the addition of nifedipine, resulted in a rapid decline in …
