Epidermal growth factor receptor is indispensable for c-Fos expression and protein synthesis by angiotensin II.
We have reported that angiotensin II induces the epidermal growth factor (EGF) receptor transactivation leading to extracellular signal-regulated kinase (ERK) activation in rat vascular smooth muscle cells. Here, we report that the EGF receptor kinase inhibitor AG1478 and the ERK kinase inhibitor PD98059 markedly inhibited angiotensin II-induced c-Fos expression and protein synthesis but not c-Jun expression in these cells. These data suggest that the EGF receptor transactivation and subsequent ERK activation are indispensable for angiotensin II-mediated growth promotion of vascular smooth muscle cells providing a new mechanistic insight whereby angiotensin II contributes abnormal vascular remodeling.
Eguchi
S
S
Department of Biochemistry, Vanderbilt University School of Medicine, Nashville, TN 37232, USA. satoru.eguchi@vanderbilt.edu
Iwasaki
H
H
Hirata
Y
Y
Frank
G D
GD
Motley
E D
ED
Yamakawa
T
T
Numaguchi
K
K
Inagami
T
T
D000818:Animals; D004815:Epidermal Growth Factor / Q000378:metabolism*; D015151:Immunoblotting; D066298:In Vitro Techniques; D009124:Muscle Proteins / Q000096:biosynthesis*; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D016760:Proto-Oncogene Proteins c-fos / Q000096:biosynthesis*; D051381:Rats; D017207:Rats, Sprague-Dawley
D009124:Muscle Proteins; D016760:Proto-Oncogene Proteins c-fos; D004815:Epidermal Growth Factor