TY - JOUR
T1 - Stimulation of 42/44kDa mitogen-activated protein kinases by arginine vasopressin in rat cardiomyocytes
AU - Aharonovitz, Orit
AU - Aboulafia-Etzion, Sharon
AU - Leor, Jonathan
AU - Alexander Battler, Battler
AU - Granot, Yosef
N1 - Funding Information:
This work was supported in part by the Gila and Arieh Keshet heart disease research fund. The technical assistance of Mrs Hanna Ben Galim is highly appreciated.
PY - 1998/1/2
Y1 - 1998/1/2
N2 - Vasoconstrictors, such as angiotensin II (Ang II), are involved in the regulatory mechanisms of post myocardial infarction (MI) hypertrophy. Arginine vasopressin (AVP), may be another vasoconstrictor that influences the mechanisms that lead to post MI hypertrophy. In these studies we investigated the possible activation of the 42/44 kDa mitogen-activated protein kinases (MAPKs), also referred as extracellular signal regulated kinases (ERKs), in cultured cardiomyocytes. Treatment of rat cardiomyocytes with AVP, Ang II and phorbol 12-myristate 13-acetate (PMA) increases the activation of ERKs. The activity of the 32/44 kDa MAPKs was tested using the phosphorylation of: (1) EGF receptor peptide (EGFR-P); (2) myelin basic protein (MBP) immobilized in poly acrylamide gels; and (3) T183 and Y185 residues of these proteins. The activity of the MAPKs, induced by AVP or PMA was inhibited by downregulation of protein kinase C (PKC), by the tyrosine kinase inhibitor genistein and by MAPK kinase (MEK) inhibitor, PD98059. In addition, the AVP-induced stimulation of MAPKs was shown to be mediated through a V, receptor. We suggest that AVP activates the 42/44 kDa MAPKs through a signal transduction pathway that involves stimulation of AVP-V1 receptor, tyrosine kinase, PKC and MEK. These results suggest that AVP may be involved in ERKs dependent regulatory functions of cardiomyocytes growth.
AB - Vasoconstrictors, such as angiotensin II (Ang II), are involved in the regulatory mechanisms of post myocardial infarction (MI) hypertrophy. Arginine vasopressin (AVP), may be another vasoconstrictor that influences the mechanisms that lead to post MI hypertrophy. In these studies we investigated the possible activation of the 42/44 kDa mitogen-activated protein kinases (MAPKs), also referred as extracellular signal regulated kinases (ERKs), in cultured cardiomyocytes. Treatment of rat cardiomyocytes with AVP, Ang II and phorbol 12-myristate 13-acetate (PMA) increases the activation of ERKs. The activity of the 32/44 kDa MAPKs was tested using the phosphorylation of: (1) EGF receptor peptide (EGFR-P); (2) myelin basic protein (MBP) immobilized in poly acrylamide gels; and (3) T183 and Y185 residues of these proteins. The activity of the MAPKs, induced by AVP or PMA was inhibited by downregulation of protein kinase C (PKC), by the tyrosine kinase inhibitor genistein and by MAPK kinase (MEK) inhibitor, PD98059. In addition, the AVP-induced stimulation of MAPKs was shown to be mediated through a V, receptor. We suggest that AVP activates the 42/44 kDa MAPKs through a signal transduction pathway that involves stimulation of AVP-V1 receptor, tyrosine kinase, PKC and MEK. These results suggest that AVP may be involved in ERKs dependent regulatory functions of cardiomyocytes growth.
KW - Arginine vasopressin
KW - Cardiomyocyte
KW - Extracellular signal regulated kinase
KW - Mitogen-activated protein kinase
KW - Protein kinase C
KW - Tyrosine kinase
UR - http://www.scopus.com/inward/record.url?scp=0032472073&partnerID=8YFLogxK
U2 - 10.1016/S0167-4889(97)00122-5
DO - 10.1016/S0167-4889(97)00122-5
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AN - SCOPUS:0032472073
SN - 0167-4889
VL - 1401
SP - 105
EP - 111
JO - Biochimica et Biophysica Acta - Molecular Cell Research
JF - Biochimica et Biophysica Acta - Molecular Cell Research
IS - 1
ER -
