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Possible role of coexpression of CD9 with membrane‐anchored heparin‐binding EGF‐like growth factor and amphiregulin in cultured human keratinocyte growth
Author(s) -
Inui Shigeki,
Higashiyama Shigeki,
Hashimoto Koji,
Higashiyama Mari,
Yoshikawa Kunihiko,
Taniguchi Naoyuki
Publication year - 1997
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/(sici)1097-4652(199706)171:3<291::aid-jcp7>3.0.co;2-j
Subject(s) - juxtacrine signalling , amphiregulin , epidermal growth factor , microbiology and biotechnology , ectodomain , growth factor , heparin binding egf like growth factor , cell growth , chemistry , biology , autocrine signalling , biochemistry , receptor
CD9 is a protein with 4 transmembrane domains, and functions as a cell surface antigen. We have previously reported that CD9 functions as an up‐regulator of membrane‐anchored heparin‐binding EGF‐like growth factor (proHB‐EGF) activity, which is a potent mitogen as well as a soluble HB‐EGF. Anti‐CD9 antibodies can neutralize the juxtacrine activity of proHB‐EGF when both CD9 and proHB‐EGF are coexpressed. We demonstrated here: (1) the CD9 gene was transcribed and translated in the cultured human keratinocytes; (2) anti‐CD9 antibody inhibited the approximately 50% growth of human keratinocytes in culture; (3) CD9 was coprecipitated with proHB‐EGF and membrane‐anchored amphiregulin (proAR), and (4) the transient coexpression of CD9 with proHB‐EGF or proAR in mouse L cells up‐regulated their juxtacrine growth factor activities. These results suggest that CD9 would make a heterodimer and/or trimer complex with proHB‐EGF and proAR, and might cooperate with proHB‐EGF and proAR for human keratinocyte growth in a juxtacrine manner. J. Cell. Physiol. 171:291–298, 1997. © 1997 Wiley‐Liss, Inc.