PMID- 8918373 OWN - NLM STAT- MEDLINE DCOM- 19961218 LR - 20071114 IS - 1044-1549 (Print) IS - 1044-1549 (Linking) VI - 15 IP - 5 DP - 1996 Nov TI - Differential regulation of airway epithelial integrins by growth factors. PG - 664-72 AB - The pattern of integrin expression on human airway epithelium changes significantly in injury or inflammation. In particular, two integrins, the fibronectin receptor, alpha 5 beta 1 and the fibronectin/tenascin receptor alpha v beta 6, are expressed at low or undetectable levels in normal airways in vivo but are induced in response to airway epithelial injury. We investigated the effects of various growth factors known to be present in the airways on the expression of constitutively expressed and inducible airway epithelial integrins using flow cytometry. In primary cultures of human airway epithelial cells, transforming growth factor-beta 1 (TGF beta 1) dramatically increased expression of alpha v beta 6 and essentially did not affect the expression of any other integrin, including alpha 5 beta 1. In contrast, epidermal growth factor (EGF) upregulated surface levels of both alpha v beta 6 and alpha 5 beta 1. Together, TGF beta 1 and EGF had an additive effect on alpha v beta 6 and alpha 5 beta 1 expression while increasing levels of alpha 2 beta 1 and decreasing expression of alpha 3 beta 1- and alpha 6-containing integrins. In contrast, the transformed airway epithelial cell line, BEAS-2B, expressed a markedly different repertoire of integrins. Integrin expression on BEAS-2B cells was not affected by any of the growth factors tested in this study. These results demonstrate that, in primary cultures of human airway epithelial cells, the pattern of integrin expression can be dramatically altered by growth factors. The inducible integrins, alpha v beta 6, and alpha 5 beta 1 are most subject to regulation by growth factors and expression of each of these can be differentially regulated. The differential regulation of the two principal fibronectin receptors on airway epithelial cells suggests that they may mediate different cellular responses to fibronectin. FAU - Wang, A AU - Wang A AD - Department of Medicine, San Francisco General Hospital, California, USA. FAU - Yokosaki, Y AU - Yokosaki Y FAU - Ferrando, R AU - Ferrando R FAU - Balmes, J AU - Balmes J FAU - Sheppard, D AU - Sheppard D LA - eng GR - HL/AI33259/HL/NHLBI NIH HHS/United States GR - HL02765-02/HL/NHLBI NIH HHS/United States GR - HL47412/HL/NHLBI NIH HHS/United States PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - Am J Respir Cell Mol Biol JT - American journal of respiratory cell and molecular biology JID - 8917225 RN - 0 (Antibodies, Monoclonal) RN - 0 (Antigens, Neoplasm) RN - 0 (Growth Substances) RN - 0 (Integrin alpha Chains) RN - 0 (Integrins) RN - 0 (Receptors, Fibronectin) RN - 0 (integrin alpha9) RN - 0 (integrin alphavbeta6) SB - IM MH - Antibodies, Monoclonal MH - *Antigens, Neoplasm MH - Bronchi/*chemistry/cytology/drug effects MH - Cell Line, Transformed MH - Cells, Cultured MH - Epithelial Cells MH - Epithelium/chemistry/drug effects MH - Growth Substances/*pharmacology MH - Humans MH - *Integrin alpha Chains MH - Integrins/*analysis MH - Receptors, Fibronectin/*analysis MH - Up-Regulation/drug effects EDAT- 1996/11/01 00:00 MHDA- 1996/11/01 00:01 CRDT- 1996/11/01 00:00 PHST- 1996/11/01 00:00 [pubmed] PHST- 1996/11/01 00:01 [medline] PHST- 1996/11/01 00:00 [entrez] AID - 10.1165/ajrcmb.15.5.8918373 [doi] PST - ppublish SO - Am J Respir Cell Mol Biol. 1996 Nov;15(5):664-72. doi: 10.1165/ajrcmb.15.5.8918373.