Proteolysis of highly polysialylated NCAM by the tissue plasminogen activator-plasmin system in rats
Tissue-type plasminogen activator (tPA), a serine protease which converts the zymogen plasminogen to the active protease plasmin, is believed to regulate neurite extension and neural cell migration by modulating extracellular metabolism. The highly polysialylated form of the neural cell adhesion mol...
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| Veröffentlicht in: | Neuroscience letters 1998-04, Vol.246 (1), p.37-40 |
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| container_title | Neuroscience letters |
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| creator | Endo, Akira Nagai, Nobuo Urano, Tetsumei Ihara, Hayato Takada, Yumiko Hashimoto, Kenji Takada, Akikazu |
| description | Tissue-type plasminogen activator (tPA), a serine protease which converts the zymogen plasminogen to the active protease plasmin, is believed to regulate neurite extension and neural cell migration by modulating extracellular metabolism. The highly polysialylated form of the neural cell adhesion molecule (NCAM-H) is strongly expressed in the developing brain and is believed to play a role in organizing the neural network. In this report, we incubated neonatal rat brain homogenates with human tPA and rat plasminogen in order to determine whether NCAM-H would be degraded. NCAM-H was degraded by plasmin which was formed from rat plasminogen by human tPA. The degradation was inhibited by the addition of plasminogen activator inhibitor type 1 (PAI-1) or aprotinin. These results suggest a possible contribution of the tPA-plasmin system to NCAM-H turnover in the developing brain. |
| doi_str_mv | 10.1016/S0304-3940(98)00204-3 |
| format | Article |
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The highly polysialylated form of the neural cell adhesion molecule (NCAM-H) is strongly expressed in the developing brain and is believed to play a role in organizing the neural network. In this report, we incubated neonatal rat brain homogenates with human tPA and rat plasminogen in order to determine whether NCAM-H would be degraded. NCAM-H was degraded by plasmin which was formed from rat plasminogen by human tPA. The degradation was inhibited by the addition of plasminogen activator inhibitor type 1 (PAI-1) or aprotinin. These results suggest a possible contribution of the tPA-plasmin system to NCAM-H turnover in the developing brain.</description><identifier>ISSN: 0304-3940</identifier><identifier>EISSN: 1872-7972</identifier><identifier>DOI: 10.1016/S0304-3940(98)00204-3</identifier><identifier>PMID: 9622202</identifier><identifier>CODEN: NELED5</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Aging ; Animals ; Animals, Newborn ; Aprotinin - pharmacology ; Biological and medical sciences ; Brain - metabolism ; Development ; Development. Senescence. Regeneration. Transplantation ; Extracellular matrix ; Fibrinolysin - metabolism ; Fundamental and applied biological sciences. Psychology ; Humans ; N-Acetylneuraminic Acid - metabolism ; Neural cell adhesion molecule ; Neural Cell Adhesion Molecules - metabolism ; Plasmin ; Plasminogen ; Plasminogen - metabolism ; Plasminogen - pharmacology ; Plasminogen Activator Inhibitor 1 - pharmacology ; Proteolysis ; Rats ; Rats, Wistar ; Time Factors ; Tissue Plasminogen Activator - metabolism ; Tissue-type plasminogen activator ; Urokinase-Type Plasminogen Activator - metabolism ; Vertebrates: nervous system and sense organs</subject><ispartof>Neuroscience letters, 1998-04, Vol.246 (1), p.37-40</ispartof><rights>1998 Elsevier Science Ireland Ltd</rights><rights>1998 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c486t-82ceec5603f45950f31472b054285e09a06d8e90ff935a87fd4a99490acdd3373</citedby><cites>FETCH-LOGICAL-c486t-82ceec5603f45950f31472b054285e09a06d8e90ff935a87fd4a99490acdd3373</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0304394098002043$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2240129$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9622202$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Endo, Akira</creatorcontrib><creatorcontrib>Nagai, Nobuo</creatorcontrib><creatorcontrib>Urano, Tetsumei</creatorcontrib><creatorcontrib>Ihara, Hayato</creatorcontrib><creatorcontrib>Takada, Yumiko</creatorcontrib><creatorcontrib>Hashimoto, Kenji</creatorcontrib><creatorcontrib>Takada, Akikazu</creatorcontrib><title>Proteolysis of highly polysialylated NCAM by the tissue plasminogen activator-plasmin system in rats</title><title>Neuroscience letters</title><addtitle>Neurosci Lett</addtitle><description>Tissue-type plasminogen activator (tPA), a serine protease which converts the zymogen plasminogen to the active protease plasmin, is believed to regulate neurite extension and neural cell migration by modulating extracellular metabolism. The highly polysialylated form of the neural cell adhesion molecule (NCAM-H) is strongly expressed in the developing brain and is believed to play a role in organizing the neural network. In this report, we incubated neonatal rat brain homogenates with human tPA and rat plasminogen in order to determine whether NCAM-H would be degraded. NCAM-H was degraded by plasmin which was formed from rat plasminogen by human tPA. The degradation was inhibited by the addition of plasminogen activator inhibitor type 1 (PAI-1) or aprotinin. These results suggest a possible contribution of the tPA-plasmin system to NCAM-H turnover in the developing brain.</description><subject>Aging</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Aprotinin - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Brain - metabolism</subject><subject>Development</subject><subject>Development. Senescence. Regeneration. Transplantation</subject><subject>Extracellular matrix</subject><subject>Fibrinolysin - metabolism</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Humans</subject><subject>N-Acetylneuraminic Acid - metabolism</subject><subject>Neural cell adhesion molecule</subject><subject>Neural Cell Adhesion Molecules - metabolism</subject><subject>Plasmin</subject><subject>Plasminogen</subject><subject>Plasminogen - metabolism</subject><subject>Plasminogen - pharmacology</subject><subject>Plasminogen Activator Inhibitor 1 - pharmacology</subject><subject>Proteolysis</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Time Factors</subject><subject>Tissue Plasminogen Activator - metabolism</subject><subject>Tissue-type plasminogen activator</subject><subject>Urokinase-Type Plasminogen Activator - metabolism</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0304-3940</issn><issn>1872-7972</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkVtr3DAQhUVpSTdpf0JAD6UkD25HsmRLTyUsvUF6gbbPQiuPsyq-bDXagP99vbtmX_M0mjOfNOIcxq4FvBMgqve_oARVlFbBjTW3APLQPWMrYWpZ1LaWz9nqjLxkl0R_AUALrS7Yha2klCBXrPmZxoxjN1EkPrZ8Gx-23cR3R8V3U-czNvz7-u4b30w8b5HnSLRHvus89XEYH3DgPuT46POYikXlNFHGns-n5DO9Yi9a3xG-XuoV-_Pp4-_1l-L-x-ev67v7IihT5cLIgBh0BWWrtNXQlkLVcgNaSaMRrIeqMWihbW2pvanbRnlrlQUfmqYs6_KKvT29u0vjvz1Sdn2kgF3nBxz35GprZa2hfBIUlRLCSDOD-gSGNBIlbN0uxd6nyQlwhxjcMQZ38NhZ444xuMOC62XBftNjc761-D7P3yxzT8F3bfJDiHTGpFQgpJ2xDycMZ9ceIyZHIeIQsIkJQ3bNGJ_4yH_T_qRQ</recordid><startdate>19980417</startdate><enddate>19980417</enddate><creator>Endo, Akira</creator><creator>Nagai, Nobuo</creator><creator>Urano, Tetsumei</creator><creator>Ihara, Hayato</creator><creator>Takada, Yumiko</creator><creator>Hashimoto, Kenji</creator><creator>Takada, Akikazu</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><scope>IQODW</scope><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>7TK</scope><scope>7X8</scope></search><sort><creationdate>19980417</creationdate><title>Proteolysis of highly polysialylated NCAM by the tissue plasminogen activator-plasmin system in rats</title><author>Endo, Akira ; Nagai, Nobuo ; Urano, Tetsumei ; Ihara, Hayato ; Takada, Yumiko ; Hashimoto, Kenji ; Takada, Akikazu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c486t-82ceec5603f45950f31472b054285e09a06d8e90ff935a87fd4a99490acdd3373</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Aging</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Aprotinin - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Brain - metabolism</topic><topic>Development</topic><topic>Development. Senescence. Regeneration. Transplantation</topic><topic>Extracellular matrix</topic><topic>Fibrinolysin - metabolism</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Humans</topic><topic>N-Acetylneuraminic Acid - metabolism</topic><topic>Neural cell adhesion molecule</topic><topic>Neural Cell Adhesion Molecules - metabolism</topic><topic>Plasmin</topic><topic>Plasminogen</topic><topic>Plasminogen - metabolism</topic><topic>Plasminogen - pharmacology</topic><topic>Plasminogen Activator Inhibitor 1 - pharmacology</topic><topic>Proteolysis</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Time Factors</topic><topic>Tissue Plasminogen Activator - metabolism</topic><topic>Tissue-type plasminogen activator</topic><topic>Urokinase-Type Plasminogen Activator - metabolism</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Endo, Akira</creatorcontrib><creatorcontrib>Nagai, Nobuo</creatorcontrib><creatorcontrib>Urano, Tetsumei</creatorcontrib><creatorcontrib>Ihara, Hayato</creatorcontrib><creatorcontrib>Takada, Yumiko</creatorcontrib><creatorcontrib>Hashimoto, Kenji</creatorcontrib><creatorcontrib>Takada, Akikazu</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neuroscience letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Endo, Akira</au><au>Nagai, Nobuo</au><au>Urano, Tetsumei</au><au>Ihara, Hayato</au><au>Takada, Yumiko</au><au>Hashimoto, Kenji</au><au>Takada, Akikazu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Proteolysis of highly polysialylated NCAM by the tissue plasminogen activator-plasmin system in rats</atitle><jtitle>Neuroscience letters</jtitle><addtitle>Neurosci Lett</addtitle><date>1998-04-17</date><risdate>1998</risdate><volume>246</volume><issue>1</issue><spage>37</spage><epage>40</epage><pages>37-40</pages><issn>0304-3940</issn><eissn>1872-7972</eissn><coden>NELED5</coden><abstract>Tissue-type plasminogen activator (tPA), a serine protease which converts the zymogen plasminogen to the active protease plasmin, is believed to regulate neurite extension and neural cell migration by modulating extracellular metabolism. The highly polysialylated form of the neural cell adhesion molecule (NCAM-H) is strongly expressed in the developing brain and is believed to play a role in organizing the neural network. In this report, we incubated neonatal rat brain homogenates with human tPA and rat plasminogen in order to determine whether NCAM-H would be degraded. NCAM-H was degraded by plasmin which was formed from rat plasminogen by human tPA. The degradation was inhibited by the addition of plasminogen activator inhibitor type 1 (PAI-1) or aprotinin. These results suggest a possible contribution of the tPA-plasmin system to NCAM-H turnover in the developing brain.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>9622202</pmid><doi>10.1016/S0304-3940(98)00204-3</doi><tpages>4</tpages></addata></record> |
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| subjects | Aging Animals Animals, Newborn Aprotinin - pharmacology Biological and medical sciences Brain - metabolism Development Development. Senescence. Regeneration. Transplantation Extracellular matrix Fibrinolysin - metabolism Fundamental and applied biological sciences. Psychology Humans N-Acetylneuraminic Acid - metabolism Neural cell adhesion molecule Neural Cell Adhesion Molecules - metabolism Plasmin Plasminogen Plasminogen - metabolism Plasminogen - pharmacology Plasminogen Activator Inhibitor 1 - pharmacology Proteolysis Rats Rats, Wistar Time Factors Tissue Plasminogen Activator - metabolism Tissue-type plasminogen activator Urokinase-Type Plasminogen Activator - metabolism Vertebrates: nervous system and sense organs |
| title | Proteolysis of highly polysialylated NCAM by the tissue plasminogen activator-plasmin system in rats |
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