TY - JOUR
T1 - Developmental changes of protein kinase C and Gsα in hypertrophic cardiomyopathic hamster hearts
AU - Cai, John J.
AU - Yu, Hongwei
AU - Lee, Hon Chi
PY - 1993/11
Y1 - 1993/11
N2 - Protein kinase C (PKC) and GTP-binding proteins (G-proteins) are known to be major determinants in the modulation of cardiac function. In this study, we examined the developmental changes of PKC and the α-subunit of the stimulatory guanosine triphosphate binding protein (Gsα) in hypertrophic cardiomyopathic Syrian hamster (BIO 14.6) hearts, before the onset of hypertrophy (30 days old) and at the peak of hypertrophy (6 months old) and compared these with age-matched control hamster (BIO RB) hearts. At 30 days, cardiac PKC activity was similar between BIO 14.6 and BIO RB both in the membrane (117.1 ± 9.9 pmol/min/mg vs 131.2 ± 12.7 pmol/min/mg in controls, n = 8) and in the cytosolic fractions (213.1 ± 22.0 pmol/min/mg vs 186.6 ± 23.9 pmol/min/mg in controls, n = 9). At 6 months, PKC activity was significantly higher in BIO 14.6 than in controls, both in the cardiac membrane (131.9 ± 7.1 pmol/min/mg vs 40.7 ± 4.7 pmol/min/mg in controls, n = 8, p < 0.00001) and cytosol (77.9 ± 2.1 pmol/min/mg vs 54.6 ± 3.3 pmol/min/mg in controls, n = 6, p < 0.0005). In BIO RB hearts, membrane and cytosolic PKC activities were significantly reduced at 6 months compared with those at 30 days of age (p < 0.001). However, the membrane PKC activity in 6-month-old BIO 14.6 was maintained at the level of the 30-day-old hearts. On the other hand, the relative immunoreactive amounts of Gsα were similar between BIO RB and BIO 14.6 hearts at 30 days and at 6 months of age. At less than 30 days, a single Gsα peptide at 45 kd was detected in both control and BIO 14.6 hearts. At 6 months of age, the presence of an additional Gsα peptide at 53 kd became apparent. These results suggest that hamster cardiac signal transducers undergo developmental changes including Gsα expression and reduction of PKC activity. Such developmental reduction in PKC activity may be impaired in hypertrophic cardiomyopathic hamster hearts.
AB - Protein kinase C (PKC) and GTP-binding proteins (G-proteins) are known to be major determinants in the modulation of cardiac function. In this study, we examined the developmental changes of PKC and the α-subunit of the stimulatory guanosine triphosphate binding protein (Gsα) in hypertrophic cardiomyopathic Syrian hamster (BIO 14.6) hearts, before the onset of hypertrophy (30 days old) and at the peak of hypertrophy (6 months old) and compared these with age-matched control hamster (BIO RB) hearts. At 30 days, cardiac PKC activity was similar between BIO 14.6 and BIO RB both in the membrane (117.1 ± 9.9 pmol/min/mg vs 131.2 ± 12.7 pmol/min/mg in controls, n = 8) and in the cytosolic fractions (213.1 ± 22.0 pmol/min/mg vs 186.6 ± 23.9 pmol/min/mg in controls, n = 9). At 6 months, PKC activity was significantly higher in BIO 14.6 than in controls, both in the cardiac membrane (131.9 ± 7.1 pmol/min/mg vs 40.7 ± 4.7 pmol/min/mg in controls, n = 8, p < 0.00001) and cytosol (77.9 ± 2.1 pmol/min/mg vs 54.6 ± 3.3 pmol/min/mg in controls, n = 6, p < 0.0005). In BIO RB hearts, membrane and cytosolic PKC activities were significantly reduced at 6 months compared with those at 30 days of age (p < 0.001). However, the membrane PKC activity in 6-month-old BIO 14.6 was maintained at the level of the 30-day-old hearts. On the other hand, the relative immunoreactive amounts of Gsα were similar between BIO RB and BIO 14.6 hearts at 30 days and at 6 months of age. At less than 30 days, a single Gsα peptide at 45 kd was detected in both control and BIO 14.6 hearts. At 6 months of age, the presence of an additional Gsα peptide at 53 kd became apparent. These results suggest that hamster cardiac signal transducers undergo developmental changes including Gsα expression and reduction of PKC activity. Such developmental reduction in PKC activity may be impaired in hypertrophic cardiomyopathic hamster hearts.
UR - http://www.scopus.com/inward/record.url?scp=0027454499&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0027454499&partnerID=8YFLogxK
M3 - Article
C2 - 8228571
AN - SCOPUS:0027454499
SN - 0022-2143
VL - 122
SP - 533
EP - 541
JO - The Journal of Laboratory and Clinical Medicine
JF - The Journal of Laboratory and Clinical Medicine
IS - 5
ER -