Controls of EGF-induced morphological transformation of human bronchial epithelial cells
| Autor: | Joe D. Beckmann, Marc P. Kai, Annette Stewart, Timothy P. Keeton |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
Physiology
medicine.drug_class Clinical Biochemistry Bronchi Respiratory Mucosa Biology Cell Line chemistry.chemical_compound Transforming Growth Factor beta Epidermal growth factor medicine Humans Pseudopodia Enzyme Inhibitors Phosphorylation Receptor Cells Cultured Myristoylation Sulfonamides Dose-Response Relationship Drug Epidermal Growth Factor Epithelial Cells Tyrosine phosphorylation Cell Biology Transforming growth factor beta Protein kinase inhibitor Isoquinolines Cell biology ErbB Receptors Kinetics Bucladesine chemistry Phorbol biology.protein Tetradecanoylphorbol Acetate Drug Antagonism hormones hormone substitutes and hormone antagonists Hormone |
| Zdroj: | Journal of Cellular Physiology. 189:171-178 |
| ISSN: | 1097-4652 0021-9541 |
| DOI: | 10.1002/jcp.10013 |
| Popis: | Human bronchial epithelial cells, both normal primary (NHBE) and the BEAS-2B line, respond to epidermal growth factor (EGF) by extruding lengthy filaments, or filapodia. The morphological transformation of BEAS-2B cells maximized at 48 h using 1–10 nM EGF. EGF-induced filapodia extension was inhibited by co-exposure to transforming growth factor beta, which did not affect tyrosine phosphorylation of the EGF receptor (EGFR). Inhibition was also effected by phorbol myristoyl acetate (PMA), which reduced the rate of EGFR tyrosine phosphorylation. Dibutyryl-cAMP had no effect, whereas the protein kinase inhibitor H-89 stimulated the EGF response. The ability to regulate cellular responses to EGF by hormonal and chemical approaches has implications for current investigations into the roles of EGF in lung growth, differentiation, and wound repair. © 2001 Wiley-Liss, Inc. |
| Databáze: | OpenAIRE |
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