{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,19]],"date-time":"2026-02-19T15:38:50Z","timestamp":1771515530054,"version":"3.50.1"},"reference-count":28,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2008,10,17]],"date-time":"2008-10-17T00:00:00Z","timestamp":1224201600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bjui-journals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["BJU International"],"published-print":{"date-parts":[[2009,2]]},"abstract":"<jats:sec>\n                    <jats:title>OBJECTIVE<\/jats:title>\n                    <jats:p>To delineate the mechanism underlying the potential functional relationship between interstitial cystitis antiproliferative factor (APF) and heparin\u2010binding epidermal growth factor\u2010like growth factor (HB\u2010EGF), as APF has previously been shown to decrease the proliferation rate of normal bladder epithelial cells and the amount of HB\u2010EGF produced by these cells.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>MATERIALS AND METHODS<\/jats:title>\n                    <jats:p>APF\u2010responsive T24 transitional carcinoma bladder cells were treated with high\u2010pressure liquid chromatography\u2010purified native APF with or without HB\u2010EGF to determine the involvement of signalling pathways and proliferation by Western blot analysis, p38 mitogen\u2010activated protein kinase (MAPK) and extracellular signal\u2010regulated kinase (Erk)\/MAPK assays, and 3\u2010(4,5\u2010dimethylthiazolyl\u20102)\u20102,5\u2010diphenyltetrazolium bromide (MTT) assay.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>Cyclic stretch induced the secretion of HB\u2010EGF from T24 cells overexpressing the HB\u2010EGF precursor, resulting in enhanced proliferation. T24 cells treated with APF had increased p38MAPK activity and suppressed cell growth, events that were both reversed by treatment with a p38MAPK\u2010selective inhibitor. Activation of Erk\/MAPK by HB\u2010EGF was inhibited by APF, and APF did not stimulate p38MAPK in the presence of soluble HB\u2010EGF or when cells overexpressed constitutively secreted HB\u2010EGF. Lastly, APF inhibitory effects on cell growth were attenuated by HB\u2010EGF.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS<\/jats:title>\n                    <jats:p>These results indicate that HB\u2010EGF and APF are functionally antagonistic and signal through parallel MAPK signalling pathways in bladder cells.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/j.1464-410x.2008.08097.x","type":"journal-article","created":{"date-parts":[[2009,1,20]],"date-time":"2009-01-20T10:43:36Z","timestamp":1232448216000},"page":"541-546","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":40,"title":["Heparin\u2010binding epidermal growth factor\u2010like growth factor functionally antagonizes interstitial cystitis antiproliferative factor via mitogen\u2010activated protein kinase pathway 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