Prorenin induces vascular smooth muscle cell proliferation and hypertrophy via epidermal growth factor receptor-mediated extracellular signal-regulated kinase and Akt activation pathway

2011 ◽  
Vol 29 (4) ◽  
pp. 696-705 ◽  
Author(s):  
Gang Liu ◽  
Hirofumi Hitomi ◽  
Naohisa Hosomi ◽  
Yuki Shibayama ◽  
Daisuke Nakano ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epidermal Growth Factor Receptor ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Akt Activation ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Epidermal Growth

T Cell–Induced Airway Smooth Muscle Cell Proliferation via the Epidermal Growth Factor Receptor

2013 ◽  
Vol 49 (4) ◽  
pp. 563-570 ◽  
Author(s):  
Saba Al Heialy ◽  
Paul-Andre Risse ◽  
Melissa A. Zeroual ◽  
Horia N. Roman ◽  
Kimitake Tsuchiya ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epidermal Growth Factor Receptor ◽  
Smooth Muscle ◽  
T Cell ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Smooth Muscle Cell ◽  
Growth Factor Receptor ◽  
Airway Smooth Muscle Cell ◽  
Epidermal Growth

scholarly journals The UV (Ribotoxic) Stress Response of Human Keratinocytes Involves the Unexpected Uncoupling of the Ras-Extracellular Signal-Regulated Kinase Signaling Cascade from the Activated Epidermal Growth Factor Receptor

2002 ◽  
Vol 22 (15) ◽  
pp. 5380-5394 ◽  
Author(s):  
Mihail S. Iordanov ◽  
Remy J. Choi ◽  
Olga P. Ryabinina ◽  
Thanh-Hoai Dinh ◽  
Robert K. Bright ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Growth Factor Receptor ◽  
Erk Signaling ◽  
Signaling Cascade ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Ribotoxic Stress Response ◽  
Epidermal Growth

ABSTRACT In mammals, UVB radiation is of biological relevance primarily for the cells of the epidermis. We report here the existence of a UVB response that is specific for proliferating human epidermal keratinocytes. Unlike other cell types that also display a UVB response, keratinocytes respond to UVB irradiation with a transient but potent downregulation of the Ras-extracellular signal-regulated kinase (ERK) signaling cascade. The downregulation of ERK precedes a profound decrease in the steady-state levels of cyclin D1, a mediator of the proliferative action of ERK. Keratinocytes exhibit high constitutive activity of the Ras-ERK signaling cascade even in culture medium lacking supplemental growth factors. The increased activity of Ras and phosphorylation of ERK in these cells are maintained by the autocrine production of secreted molecules that activate the epidermal growth factor receptor (EGFR). Irradiation of keratinocytes increases the phosphorylation of EGFR on tyrosine residues Y845, Y992, Y1045, Y1068, Y1086, Y1148, and Y1173 above the basal levels and leads to the increased recruitment of the adaptor proteins Grb2 and ShcA and of a p55 form of the regulatory subunit of the phosphatidylinositide 3-kinase to the UVB-activated EGFR. Paradoxically, however, UVB causes, at the same time, the inactivation of Ras and a subsequent dephosphorylation of ERK. By contrast, the signaling pathway leading from the activated EGFR to the phosphorylation of PKB/Akt1 is potentiated by UVB. The UVB response of keratinocytes appeared to be a manifestation of the more general ribotoxic stress response inasmuch as the transduction of the UVB-generated inhibitory signal to Ras and ERK required the presence of active ribosomes at the time of irradiation.

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