Beckmann J D, Stewart A, Kai M, Keeton T P
Department of Biochemistry, Alma College, Alma, Michigan 48801, USA.
J Cell Physiol. 2001 Nov;189(2):171-8. doi: 10.1002/jcp.10013.
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.
人支气管上皮细胞，包括正常原代细胞（NHBE）和BEAS-2B细胞系，对表皮生长因子（EGF）的反应是伸出细长的丝状伪足。使用1-10 nM EGF时，BEAS-2B细胞的形态转化在48小时达到最大值。同时暴露于转化生长因子β可抑制EGF诱导的丝状伪足延伸，而这并不影响表皮生长因子受体（EGFR）的酪氨酸磷酸化。佛波醇肉豆蔻酸酯乙酸酯（PMA）也有抑制作用，它降低了EGFR酪氨酸磷酸化的速率。二丁酰环磷腺苷（Dibutyryl-cAMP）没有作用，而蛋白激酶抑制剂H-89则刺激了EGF反应。通过激素和化学方法调节细胞对EGF反应的能力，对目前关于EGF在肺生长、分化和伤口修复中作用的研究具有重要意义。
