Faculty Opinions recommendation of G protein coupling and second messenger generation are indispensable for metalloprotease-dependent, heparin-binding epidermal growth factor shedding through angiotensin II type-1 receptor.

2005 ◽  
Author(s):  
Judith White
Keyword(s):  
Angiotensin Ii ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
G Protein ◽  
Second Messenger ◽  
Heparin Binding ◽  
G Protein Coupling ◽  
Protein Coupling ◽  
Epidermal Growth

scholarly journals Differential Pathways of Angiotensin II-Induced Extracellularly Regulated Kinase 1/2 Phosphorylation in Specific Cell Types: Role of Heparin-Binding Epidermal Growth Factor

2004 ◽  
Vol 18 (8) ◽  
pp. 2035-2048 ◽  
Author(s):  
Bukhtiar H. Shah ◽  
Akin Yesilkaya ◽  
J. Alberto Olivares-Reyes ◽  
Hung-Dar Chen ◽  
László Hunyady ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cell Types ◽  
Specific Cell ◽  
Heparin Binding ◽  
Epidermal Growth

Heparin-binding epidermal growth factor (EGF)-like growth factor in pediatric patients with type 1 diabetes mellitus

2020 ◽  
Vol 38 (2) ◽  
pp. 120-126
Author(s):  
Dragana Kacarevic ◽  
Natasa Bogavac-Stanojevic ◽  
Vesna Spasojevic-Kalimanovska ◽  
Dragana Bojanin ◽  
Tatjana Milenkovic ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Type 1 Diabetes Mellitus ◽  
Pediatric Patients ◽  
Heparin Binding ◽  
Epidermal Growth

17β-Estradiol enhances heparin-binding epidermal growth factor-like growth factor production in human keratinocytes

2005 ◽  
Vol 288 (4) ◽  
pp. C813-C823 ◽  
Author(s):  
Naoko Kanda ◽  
Shinichi Watanabe
Keyword(s):  
Estrogen Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
G Protein ◽  
Transcriptional Activity ◽  
Human Keratinocytes ◽  
Heparin Binding ◽  
17Β Estradiol ◽  
Epidermal Growth

Heparin-binding epidermal growth factor-like growth factor (HB-EGF) enhances reepithelialization in wounds. Estrogen is known to promote cutaneous wound repair. We examined the in vitro effects of 17β-estradiol (E2) on HB-EGF production by human keratinocytes. E2 or membrane-impermeable BSA-conjugated E2 (E2-BSA) increased HB-EGF secretion, mRNA level, and promoter activity in keratinocytes. E2 or E2-BSA enhanced in vitro wound closure in keratinocytes, and the closure was suppressed by anti-HB-EGF antibody. Activator protein-1 (AP-1) and specificity protein 1 (Sp1) sites on HB-EGF promoter were responsible for the E2- or E2-BSA-induced transactivation. Antisense oligonucleotides against c-Fos, c-Jun, and Sp1 blocked E2- or E2-BSA-induced HB-EGF transactivation. E2 or E2-BSA enhanced DNA binding and transcriptional activity of AP-1 and generated c-Fos/c-Jun heterodimers by inducing c-Fos expression. E2 or E2-BSA enhanced DNA binding and transcriptional activity of Sp1 in parallel with the enhancement of Sp1 phosphorylation. These effects of E2 or E2-BSA were not blocked by the nuclear estrogen receptor antagonist ICI-182,780 or anti-estrogen receptor-α or -β antibodies but were blocked by inhibitors of G protein, phosphatidylinositol-specific PLC, PKC-α, and MEK1. These results suggest that E2 or E2-BSA may enhance HB-EGF production via activation of AP-1 and Sp1. These effects of E2 or E2-BSA may be dependent on membrane G protein-coupled receptors different from nuclear estrogen receptors and on the receptor-mediated activities of phosphatidylinositol-specific PLC, PKC-α, and MEK1. E2 may enhance wound reepithelialization by promoting HB-EGF production in keratinocytes.

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