Extracellular Matrix-dependent Activation of Syndecan-1 Expression in Keratinocyte Growth Factor-treated Keratinocytes

Syndecan-1 is a major heparan sulfate proteoglycan of the epidermis. Its expression is strongly induced in migrating and proliferating keratinocytes during wound healing and, on the other hand, diminished or lost in invasive squamous cell carcinoma. We have recently found in the syndecan-1 gene an e...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:The Journal of biological chemistry 1999-04, Vol.274 (14), p.9891-9898
Hauptverfasser: Määttä, A, Jaakkola, P, Jalkanen, M
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 9898
container_issue 14
container_start_page 9891
container_title The Journal of biological chemistry
container_volume 274
creator Määttä, A
Jaakkola, P
Jalkanen, M
description Syndecan-1 is a major heparan sulfate proteoglycan of the epidermis. Its expression is strongly induced in migrating and proliferating keratinocytes during wound healing and, on the other hand, diminished or lost in invasive squamous cell carcinoma. We have recently found in the syndecan-1 gene an enhancer (fibroblast growth factor-inducible response element (FiRE)) that activates gene expression in wound edge keratinocytes (Jaakkola, P., Kontusaari, S., Kauppi, T., Määttä, A., and Jalkanen, M. (1998) FASEB J. 12, 959–969). Now, we demonstrate that the activation of this enhancer by keratinocyte growth factor (KGF) is modulated by the components of the extracellular matrix (ECM). MCA-3D mouse immortal keratinocytes growing on fibrillar collagen failed to activate FiRE and subsequently to induce syndecan-1 in response to KGF. The same cells growing on fibronectin or laminin, however, increased FiRE-dependent reporter gene expression upon KGF treatment. The inhibition of the KGF induction by collagen appears to be specific for signaling to FiRE, as the increase in cell proliferation by KGF was not affected. The effect was selective to KGF, as EGF-induction was independent on ECM composition. Changes in the transcription factor binding were not involved in the differential activation of FiRE, as the levels and composition of the AP-1 complexes were unchanged. However, application of anisomycin, an activator of Jun amino-terminal kinase, resulted in a lower response in cells growing on collagen compared with fibronectin. These results indicate that the composition of ECM and availability of growth factors can play a role in the epidermal regulation of syndecan-1 expression and that FiRE is a novel target for gene regulation by the extracellular matrix.
doi_str_mv 10.1074/jbc.274.14.9891
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_69651543</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>69651543</sourcerecordid><originalsourceid>FETCH-LOGICAL-c393t-5aa0f7b2a1ec75633a8d1fa8f4f2370cf5ddd1aca115465760450e86c59470bc3</originalsourceid><addsrcrecordid>eNqFkUFPGzEQRq2KqqSUMze0EhK3DZ61vbs-IhSgKlUPUImbNeudJUbJOtgOJP8eR-FQTp3LSDNvPmn0GDsBPgXeyIvnzk6rRk5BTnWr4QubAG9FKRQ8HrAJ5xWUulLtIfse4zPPJTV8Y4fAua7qFibsdbZJAS0tFusFhuI3puA2ZU8rGnsaU3Fpk3vF5PxY-KG43-apxbGEYrZZBYpxt3Bj8YtChkZvt4mKm-Df0ry4Rpt8KFMgTNR_QuIP9nXARaTjj37E_l7PHq5uy7s_Nz-vLu9KK7RIpULkQ9NVCGQbVQuBbQ8DtoMcKtFwO6i-7wEtAihZq6bmUnFqa6u0bHhnxRE73-eugn9ZU0xm6eLuWxzJr6Opda3yqfgvCA1oaCuZwYs9aIOPMdBgVsEtMWwNcLNzYrITk50YkGbnJF-cfkSvuyX1__B7CRk42wNz9zR_c4FM57yd0_JTzDukKpWq</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>17191824</pqid></control><display><type>article</type><title>Extracellular Matrix-dependent Activation of Syndecan-1 Expression in Keratinocyte Growth Factor-treated Keratinocytes</title><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Määttä, A ; Jaakkola, P ; Jalkanen, M</creator><creatorcontrib>Määttä, A ; Jaakkola, P ; Jalkanen, M</creatorcontrib><description>Syndecan-1 is a major heparan sulfate proteoglycan of the epidermis. Its expression is strongly induced in migrating and proliferating keratinocytes during wound healing and, on the other hand, diminished or lost in invasive squamous cell carcinoma. We have recently found in the syndecan-1 gene an enhancer (fibroblast growth factor-inducible response element (FiRE)) that activates gene expression in wound edge keratinocytes (Jaakkola, P., Kontusaari, S., Kauppi, T., Määttä, A., and Jalkanen, M. (1998) FASEB J. 12, 959–969). Now, we demonstrate that the activation of this enhancer by keratinocyte growth factor (KGF) is modulated by the components of the extracellular matrix (ECM). MCA-3D mouse immortal keratinocytes growing on fibrillar collagen failed to activate FiRE and subsequently to induce syndecan-1 in response to KGF. The same cells growing on fibronectin or laminin, however, increased FiRE-dependent reporter gene expression upon KGF treatment. The inhibition of the KGF induction by collagen appears to be specific for signaling to FiRE, as the increase in cell proliferation by KGF was not affected. The effect was selective to KGF, as EGF-induction was independent on ECM composition. Changes in the transcription factor binding were not involved in the differential activation of FiRE, as the levels and composition of the AP-1 complexes were unchanged. However, application of anisomycin, an activator of Jun amino-terminal kinase, resulted in a lower response in cells growing on collagen compared with fibronectin. These results indicate that the composition of ECM and availability of growth factors can play a role in the epidermal regulation of syndecan-1 expression and that FiRE is a novel target for gene regulation by the extracellular matrix.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.274.14.9891</identifier><identifier>PMID: 10092681</identifier><language>eng</language><publisher>United States: American Society for Biochemistry and Molecular Biology</publisher><subject>Animals ; Cell Division ; Cells, Cultured ; Collagen - metabolism ; DNA - metabolism ; Enhancer Elements, Genetic ; Epidermal Growth Factor - metabolism ; Extracellular Matrix - metabolism ; Fibroblast Growth Factor 10 ; Fibroblast Growth Factor 7 ; Fibroblast Growth Factors - biosynthesis ; Fibroblast Growth Factors - genetics ; Fibronectins - metabolism ; Growth Substances - pharmacology ; Keratinocytes - drug effects ; Keratinocytes - metabolism ; Membrane Glycoproteins - biosynthesis ; Membrane Glycoproteins - genetics ; Mice ; Proteoglycans - biosynthesis ; Proteoglycans - genetics ; Syndecan-1 ; Syndecans ; Transcription, Genetic ; Transforming Growth Factor alpha - metabolism</subject><ispartof>The Journal of biological chemistry, 1999-04, Vol.274 (14), p.9891-9898</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c393t-5aa0f7b2a1ec75633a8d1fa8f4f2370cf5ddd1aca115465760450e86c59470bc3</citedby><cites>FETCH-LOGICAL-c393t-5aa0f7b2a1ec75633a8d1fa8f4f2370cf5ddd1aca115465760450e86c59470bc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10092681$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Määttä, A</creatorcontrib><creatorcontrib>Jaakkola, P</creatorcontrib><creatorcontrib>Jalkanen, M</creatorcontrib><title>Extracellular Matrix-dependent Activation of Syndecan-1 Expression in Keratinocyte Growth Factor-treated Keratinocytes</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>Syndecan-1 is a major heparan sulfate proteoglycan of the epidermis. Its expression is strongly induced in migrating and proliferating keratinocytes during wound healing and, on the other hand, diminished or lost in invasive squamous cell carcinoma. We have recently found in the syndecan-1 gene an enhancer (fibroblast growth factor-inducible response element (FiRE)) that activates gene expression in wound edge keratinocytes (Jaakkola, P., Kontusaari, S., Kauppi, T., Määttä, A., and Jalkanen, M. (1998) FASEB J. 12, 959–969). Now, we demonstrate that the activation of this enhancer by keratinocyte growth factor (KGF) is modulated by the components of the extracellular matrix (ECM). MCA-3D mouse immortal keratinocytes growing on fibrillar collagen failed to activate FiRE and subsequently to induce syndecan-1 in response to KGF. The same cells growing on fibronectin or laminin, however, increased FiRE-dependent reporter gene expression upon KGF treatment. The inhibition of the KGF induction by collagen appears to be specific for signaling to FiRE, as the increase in cell proliferation by KGF was not affected. The effect was selective to KGF, as EGF-induction was independent on ECM composition. Changes in the transcription factor binding were not involved in the differential activation of FiRE, as the levels and composition of the AP-1 complexes were unchanged. However, application of anisomycin, an activator of Jun amino-terminal kinase, resulted in a lower response in cells growing on collagen compared with fibronectin. These results indicate that the composition of ECM and availability of growth factors can play a role in the epidermal regulation of syndecan-1 expression and that FiRE is a novel target for gene regulation by the extracellular matrix.</description><subject>Animals</subject><subject>Cell Division</subject><subject>Cells, Cultured</subject><subject>Collagen - metabolism</subject><subject>DNA - metabolism</subject><subject>Enhancer Elements, Genetic</subject><subject>Epidermal Growth Factor - metabolism</subject><subject>Extracellular Matrix - metabolism</subject><subject>Fibroblast Growth Factor 10</subject><subject>Fibroblast Growth Factor 7</subject><subject>Fibroblast Growth Factors - biosynthesis</subject><subject>Fibroblast Growth Factors - genetics</subject><subject>Fibronectins - metabolism</subject><subject>Growth Substances - pharmacology</subject><subject>Keratinocytes - drug effects</subject><subject>Keratinocytes - metabolism</subject><subject>Membrane Glycoproteins - biosynthesis</subject><subject>Membrane Glycoproteins - genetics</subject><subject>Mice</subject><subject>Proteoglycans - biosynthesis</subject><subject>Proteoglycans - genetics</subject><subject>Syndecan-1</subject><subject>Syndecans</subject><subject>Transcription, Genetic</subject><subject>Transforming Growth Factor alpha - metabolism</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUFPGzEQRq2KqqSUMze0EhK3DZ61vbs-IhSgKlUPUImbNeudJUbJOtgOJP8eR-FQTp3LSDNvPmn0GDsBPgXeyIvnzk6rRk5BTnWr4QubAG9FKRQ8HrAJ5xWUulLtIfse4zPPJTV8Y4fAua7qFibsdbZJAS0tFusFhuI3puA2ZU8rGnsaU3Fpk3vF5PxY-KG43-apxbGEYrZZBYpxt3Bj8YtChkZvt4mKm-Df0ry4Rpt8KFMgTNR_QuIP9nXARaTjj37E_l7PHq5uy7s_Nz-vLu9KK7RIpULkQ9NVCGQbVQuBbQ8DtoMcKtFwO6i-7wEtAihZq6bmUnFqa6u0bHhnxRE73-eugn9ZU0xm6eLuWxzJr6Opda3yqfgvCA1oaCuZwYs9aIOPMdBgVsEtMWwNcLNzYrITk50YkGbnJF-cfkSvuyX1__B7CRk42wNz9zR_c4FM57yd0_JTzDukKpWq</recordid><startdate>19990402</startdate><enddate>19990402</enddate><creator>Määttä, A</creator><creator>Jaakkola, P</creator><creator>Jalkanen, M</creator><general>American Society for Biochemistry and Molecular Biology</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TM</scope><scope>7X8</scope></search><sort><creationdate>19990402</creationdate><title>Extracellular Matrix-dependent Activation of Syndecan-1 Expression in Keratinocyte Growth Factor-treated Keratinocytes</title><author>Määttä, A ; Jaakkola, P ; Jalkanen, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c393t-5aa0f7b2a1ec75633a8d1fa8f4f2370cf5ddd1aca115465760450e86c59470bc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>Cell Division</topic><topic>Cells, Cultured</topic><topic>Collagen - metabolism</topic><topic>DNA - metabolism</topic><topic>Enhancer Elements, Genetic</topic><topic>Epidermal Growth Factor - metabolism</topic><topic>Extracellular Matrix - metabolism</topic><topic>Fibroblast Growth Factor 10</topic><topic>Fibroblast Growth Factor 7</topic><topic>Fibroblast Growth Factors - biosynthesis</topic><topic>Fibroblast Growth Factors - genetics</topic><topic>Fibronectins - metabolism</topic><topic>Growth Substances - pharmacology</topic><topic>Keratinocytes - drug effects</topic><topic>Keratinocytes - metabolism</topic><topic>Membrane Glycoproteins - biosynthesis</topic><topic>Membrane Glycoproteins - genetics</topic><topic>Mice</topic><topic>Proteoglycans - biosynthesis</topic><topic>Proteoglycans - genetics</topic><topic>Syndecan-1</topic><topic>Syndecans</topic><topic>Transcription, Genetic</topic><topic>Transforming Growth Factor alpha - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Määttä, A</creatorcontrib><creatorcontrib>Jaakkola, P</creatorcontrib><creatorcontrib>Jalkanen, M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of biological chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Määttä, A</au><au>Jaakkola, P</au><au>Jalkanen, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Extracellular Matrix-dependent Activation of Syndecan-1 Expression in Keratinocyte Growth Factor-treated Keratinocytes</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>1999-04-02</date><risdate>1999</risdate><volume>274</volume><issue>14</issue><spage>9891</spage><epage>9898</epage><pages>9891-9898</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><abstract>Syndecan-1 is a major heparan sulfate proteoglycan of the epidermis. Its expression is strongly induced in migrating and proliferating keratinocytes during wound healing and, on the other hand, diminished or lost in invasive squamous cell carcinoma. We have recently found in the syndecan-1 gene an enhancer (fibroblast growth factor-inducible response element (FiRE)) that activates gene expression in wound edge keratinocytes (Jaakkola, P., Kontusaari, S., Kauppi, T., Määttä, A., and Jalkanen, M. (1998) FASEB J. 12, 959–969). Now, we demonstrate that the activation of this enhancer by keratinocyte growth factor (KGF) is modulated by the components of the extracellular matrix (ECM). MCA-3D mouse immortal keratinocytes growing on fibrillar collagen failed to activate FiRE and subsequently to induce syndecan-1 in response to KGF. The same cells growing on fibronectin or laminin, however, increased FiRE-dependent reporter gene expression upon KGF treatment. The inhibition of the KGF induction by collagen appears to be specific for signaling to FiRE, as the increase in cell proliferation by KGF was not affected. The effect was selective to KGF, as EGF-induction was independent on ECM composition. Changes in the transcription factor binding were not involved in the differential activation of FiRE, as the levels and composition of the AP-1 complexes were unchanged. However, application of anisomycin, an activator of Jun amino-terminal kinase, resulted in a lower response in cells growing on collagen compared with fibronectin. These results indicate that the composition of ECM and availability of growth factors can play a role in the epidermal regulation of syndecan-1 expression and that FiRE is a novel target for gene regulation by the extracellular matrix.</abstract><cop>United States</cop><pub>American Society for Biochemistry and Molecular Biology</pub><pmid>10092681</pmid><doi>10.1074/jbc.274.14.9891</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 0021-9258
ispartof The Journal of biological chemistry, 1999-04, Vol.274 (14), p.9891-9898
issn 0021-9258
1083-351X
language eng
recordid cdi_proquest_miscellaneous_69651543
source MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection
subjects Animals
Cell Division
Cells, Cultured
Collagen - metabolism
DNA - metabolism
Enhancer Elements, Genetic
Epidermal Growth Factor - metabolism
Extracellular Matrix - metabolism
Fibroblast Growth Factor 10
Fibroblast Growth Factor 7
Fibroblast Growth Factors - biosynthesis
Fibroblast Growth Factors - genetics
Fibronectins - metabolism
Growth Substances - pharmacology
Keratinocytes - drug effects
Keratinocytes - metabolism
Membrane Glycoproteins - biosynthesis
Membrane Glycoproteins - genetics
Mice
Proteoglycans - biosynthesis
Proteoglycans - genetics
Syndecan-1
Syndecans
Transcription, Genetic
Transforming Growth Factor alpha - metabolism
title Extracellular Matrix-dependent Activation of Syndecan-1 Expression in Keratinocyte Growth Factor-treated Keratinocytes
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-24T01%3A57%3A46IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Extracellular%20Matrix-dependent%20Activation%20of%20Syndecan-1%20Expression%20in%20Keratinocyte%20Growth%20Factor-treated%20Keratinocytes&rft.jtitle=The%20Journal%20of%20biological%20chemistry&rft.au=M%C3%A4%C3%A4tt%C3%A4,%20A&rft.date=1999-04-02&rft.volume=274&rft.issue=14&rft.spage=9891&rft.epage=9898&rft.pages=9891-9898&rft.issn=0021-9258&rft.eissn=1083-351X&rft_id=info:doi/10.1074/jbc.274.14.9891&rft_dat=%3Cproquest_cross%3E69651543%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=17191824&rft_id=info:pmid/10092681&rfr_iscdi=true