{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,3]],"date-time":"2026-05-03T12:33:00Z","timestamp":1777811580810,"version":"3.51.4"},"reference-count":34,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2002,4,1]],"date-time":"2002-04-01T00:00:00Z","timestamp":1017619200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Dent Res"],"published-print":{"date-parts":[[2002,4]]},"abstract":"<jats:p>Basic fibroblast growth factor (bFGF) modulates gingival growth, and its release from heparan sulfate (HS) in the extracellular matrix (ECM) governs local tissue bioavailability. We identified a heparin\/HS interacting protein (HIP\/L29) that recognizes specific HS sequences. We hypothesize that HIP\/L29, by modulating the interactions of bFGF with HS chains on proteoglycans, could regulate bFGF bioavailability. To investigate interactions between bFGF and HIP\/L29, we isolated and cultured fibroblasts from normal gingiva and overgrown gingiva from patients on cyclosporine (CSA). bFGF significantly stimulated gingival fibroblast proliferation with or without heparin. Recombinant human HIP\/L29 dramatically decreased bFGF-induced proliferation, but did not alter responses to insulin-like growth factor-1 (IGF-1). Analysis of mitogen-activated protein kinase (MAPK) phosphorylation patterns showed that bFGF stimulation of p44 (Erk-1), but not p42 (Erk-2), also was inhibited by HIP\/L29 in a dose-dependent manner. Together, these results support our hypothesis that HIP\/L29 modulates the bioavailability and action of bFGF.<\/jats:p>","DOI":"10.1177\/154405910208100405","type":"journal-article","created":{"date-parts":[[2009,1,8]],"date-time":"2009-01-08T19:39:42Z","timestamp":1231443582000},"page":"247-252","source":"Crossref","is-referenced-by-count":10,"title":["Heparan Sulfate Interacting Protein (HIP\/L29) Negatively Regulates Growth Responses to Basic Fibroblast Growth Factor in Gingival Fibroblasts"],"prefix":"10.1177","volume":"81","author":[{"given":"T.-V.","family":"Ta","sequence":"first","affiliation":[{"name":"Department of Biological Sciences, University of Delaware, Newark, DE 19716; and"},{"name":"Department of Periodontics, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA 19104;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D.","family":"Baraniak","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences, University of Delaware, Newark, DE 19716; and"},{"name":"Department of Periodontics, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA 19104;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J.","family":"Julian","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences, University of Delaware, Newark, DE 19716; and"},{"name":"Department of Periodontics, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA 19104;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J.","family":"Korostoff","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences, University of Delaware, Newark, DE 19716; and"},{"name":"Department of Periodontics, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA 19104;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D.D.","family":"Carson","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences, University of Delaware, Newark, DE 19716; and"},{"name":"Department of Periodontics, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA 19104;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M.C.","family":"Farach-Carson","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences, University of Delaware, Newark, DE 19716; and"},{"name":"Department of Periodontics, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA 19104;"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2002,4,1]]},"reference":[{"key":"BARBER-ETAL-1992","doi-asserted-by":"publisher","DOI":"10.1902\/jop.1992.63.5.397"},{"key":"BARTOLD-1989","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0765.1989.tb00876.x"},{"key":"BRUNIUS-AND-MODEER-1989","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0714.1989.tb01348.x"},{"key":"CHANG-AND-MEIENHOFER-1978","doi-asserted-by":"publisher","DOI":"10.1111\/j.1399-3011.1978.tb02845.x"},{"key":"CHANG-ETAL-2000","doi-asserted-by":"publisher","DOI":"10.1096\/fasebj.14.1.137"},{"key":"DILL-ETAL-1993","doi-asserted-by":"publisher","DOI":"10.1902\/jop.1993.64.3.169"},{"key":"FRISKOPP-ETAL-1986","doi-asserted-by":"crossref","unstructured":"Friskopp J, Engstr\u00f6m P-E, Sundqvist K-G -1986- Characterization of mononuclear cells in cyclosporine A induced gingival enlargement. 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