Osteopontin-Deficient Bone Cells Are Defective in Their Ability to Produce NO in Response to Pulsatile Fluid Flow
Osteopontin (OPN) is a noncollagenous component of bone matrix. It mediates cell attachment and activates signal transduction pathways. In this work, bone cells, cultured from fragments of long bones derived from wild-type and OPN−/− (“knock-out”) mice, were exposed to pulsatile fluid flow (PFF) ove...
Gespeichert in:
| Veröffentlicht in: | Biochemical and biophysical research communications 2001-10, Vol.288 (2), p.448-453 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 453 |
|---|---|
| container_issue | 2 |
| container_start_page | 448 |
| container_title | Biochemical and biophysical research communications |
| container_volume | 288 |
| creator | Denhardt, D.T. Burger, E.H. Kazanecki, C. Krishna, S. Semeins, C.M. Klein-Nulend, J. |
| description | Osteopontin (OPN) is a noncollagenous component of bone matrix. It mediates cell attachment and activates signal transduction pathways. In this work, bone cells, cultured from fragments of long bones derived from wild-type and OPN−/− (“knock-out”) mice, were exposed to pulsatile fluid flow (PFF) over a 60-min period. The medium was assayed periodically for nitric oxide (NO) and prostaglandin E2 (PGE2) release. OPN+/+ cells exhibited a peak of NO production 5–10 min after the onset of PFF, decreasing to a stable plateau at 15 min; much less NO was produced by the OPN−/− cells. PFF resulted in reduced PGE2 release by both cell types, although the reduction was less for the OPN−/− cells in the 15–30 min window. Both cell types exhibited a similar enhancement of cyclooxygenase2 mRNA levels 60 min after initiation of PFF. These results suggest that bone cells require OPN to respond fully to PFF as assessed by increased NO and reduced PGE2 synthesis. |
| doi_str_mv | 10.1006/bbrc.2001.5780 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_72210702</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0006291X01957808</els_id><sourcerecordid>18186946</sourcerecordid><originalsourceid>FETCH-LOGICAL-c371t-239e7687bb7ae93793e93f1e7b4f6abbaaf59ca0f505306ef1b3f9ea811e8a623</originalsourceid><addsrcrecordid>eNqFkc1rGzEQxUVJaZyk1x6DTrmto9m1pdXRcfMFoS4hhd6EpB1RlfXKkbQp-e-jrQ09hSIYHd5vHsx7hHwBNgfG-KUx0c5rxmC-FC37QGbAJKtqYIsjMmOFqGoJP4_JSUq_CwULLj-RYwDOymtm5HmTMoZdGLIfqq_ovPU4ZHoVBqRr7PtEVxFpEdBm_4LUD_TpF_pIV8b3Pr_SHOj3GLrRIv22meRHTMUu4V9l7JPOvkd604--KzP8OSMfne4Tfj78p-THzfXT-q562Nzer1cPlW0E5KpuJAreCmOERtkI2ZTpAIVZOK6N0dotpdXMLdmyYRwdmMZJ1C0AtprXzSm52PvuYngeMWW19cmWk_SAYUxK1CUlwf4PQgstlwtewPketDGkFNGpXfRbHV8VMDW1oaY21NSGmtooC-cH59FssfuHH-IvQLsHsATx4jGqNOVvsfOxBK664N_zfgND4Zkj</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>18186946</pqid></control><display><type>article</type><title>Osteopontin-Deficient Bone Cells Are Defective in Their Ability to Produce NO in Response to Pulsatile Fluid Flow</title><source>MEDLINE</source><source>Access via ScienceDirect (Elsevier)</source><creator>Denhardt, D.T. ; Burger, E.H. ; Kazanecki, C. ; Krishna, S. ; Semeins, C.M. ; Klein-Nulend, J.</creator><creatorcontrib>Denhardt, D.T. ; Burger, E.H. ; Kazanecki, C. ; Krishna, S. ; Semeins, C.M. ; Klein-Nulend, J.</creatorcontrib><description>Osteopontin (OPN) is a noncollagenous component of bone matrix. It mediates cell attachment and activates signal transduction pathways. In this work, bone cells, cultured from fragments of long bones derived from wild-type and OPN−/− (“knock-out”) mice, were exposed to pulsatile fluid flow (PFF) over a 60-min period. The medium was assayed periodically for nitric oxide (NO) and prostaglandin E2 (PGE2) release. OPN+/+ cells exhibited a peak of NO production 5–10 min after the onset of PFF, decreasing to a stable plateau at 15 min; much less NO was produced by the OPN−/− cells. PFF resulted in reduced PGE2 release by both cell types, although the reduction was less for the OPN−/− cells in the 15–30 min window. Both cell types exhibited a similar enhancement of cyclooxygenase2 mRNA levels 60 min after initiation of PFF. These results suggest that bone cells require OPN to respond fully to PFF as assessed by increased NO and reduced PGE2 synthesis.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1006/bbrc.2001.5780</identifier><identifier>PMID: 11606063</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Bone and Bones - cytology ; Bone and Bones - metabolism ; cyclooxygenase ; cyclooxygenase 2 ; fluid flow ; mechanotransduction ; Mice ; nitric oxide ; Nitric Oxide - metabolism ; osteoblast ; osteocyte ; Osteopontin ; prostaglandin ; Pulsatile Flow - physiology ; Sialoglycoproteins - deficiency ; Sialoglycoproteins - metabolism ; Signal Transduction</subject><ispartof>Biochemical and biophysical research communications, 2001-10, Vol.288 (2), p.448-453</ispartof><rights>2001 Academic Press</rights><rights>Copyright 2001 Academic Press.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c371t-239e7687bb7ae93793e93f1e7b4f6abbaaf59ca0f505306ef1b3f9ea811e8a623</citedby><cites>FETCH-LOGICAL-c371t-239e7687bb7ae93793e93f1e7b4f6abbaaf59ca0f505306ef1b3f9ea811e8a623</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1006/bbrc.2001.5780$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11606063$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Denhardt, D.T.</creatorcontrib><creatorcontrib>Burger, E.H.</creatorcontrib><creatorcontrib>Kazanecki, C.</creatorcontrib><creatorcontrib>Krishna, S.</creatorcontrib><creatorcontrib>Semeins, C.M.</creatorcontrib><creatorcontrib>Klein-Nulend, J.</creatorcontrib><title>Osteopontin-Deficient Bone Cells Are Defective in Their Ability to Produce NO in Response to Pulsatile Fluid Flow</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>Osteopontin (OPN) is a noncollagenous component of bone matrix. It mediates cell attachment and activates signal transduction pathways. In this work, bone cells, cultured from fragments of long bones derived from wild-type and OPN−/− (“knock-out”) mice, were exposed to pulsatile fluid flow (PFF) over a 60-min period. The medium was assayed periodically for nitric oxide (NO) and prostaglandin E2 (PGE2) release. OPN+/+ cells exhibited a peak of NO production 5–10 min after the onset of PFF, decreasing to a stable plateau at 15 min; much less NO was produced by the OPN−/− cells. PFF resulted in reduced PGE2 release by both cell types, although the reduction was less for the OPN−/− cells in the 15–30 min window. Both cell types exhibited a similar enhancement of cyclooxygenase2 mRNA levels 60 min after initiation of PFF. These results suggest that bone cells require OPN to respond fully to PFF as assessed by increased NO and reduced PGE2 synthesis.</description><subject>Animals</subject><subject>Bone and Bones - cytology</subject><subject>Bone and Bones - metabolism</subject><subject>cyclooxygenase</subject><subject>cyclooxygenase 2</subject><subject>fluid flow</subject><subject>mechanotransduction</subject><subject>Mice</subject><subject>nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>osteoblast</subject><subject>osteocyte</subject><subject>Osteopontin</subject><subject>prostaglandin</subject><subject>Pulsatile Flow - physiology</subject><subject>Sialoglycoproteins - deficiency</subject><subject>Sialoglycoproteins - metabolism</subject><subject>Signal Transduction</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1rGzEQxUVJaZyk1x6DTrmto9m1pdXRcfMFoS4hhd6EpB1RlfXKkbQp-e-jrQ09hSIYHd5vHsx7hHwBNgfG-KUx0c5rxmC-FC37QGbAJKtqYIsjMmOFqGoJP4_JSUq_CwULLj-RYwDOymtm5HmTMoZdGLIfqq_ovPU4ZHoVBqRr7PtEVxFpEdBm_4LUD_TpF_pIV8b3Pr_SHOj3GLrRIv22meRHTMUu4V9l7JPOvkd604--KzP8OSMfne4Tfj78p-THzfXT-q562Nzer1cPlW0E5KpuJAreCmOERtkI2ZTpAIVZOK6N0dotpdXMLdmyYRwdmMZJ1C0AtprXzSm52PvuYngeMWW19cmWk_SAYUxK1CUlwf4PQgstlwtewPketDGkFNGpXfRbHV8VMDW1oaY21NSGmtooC-cH59FssfuHH-IvQLsHsATx4jGqNOVvsfOxBK664N_zfgND4Zkj</recordid><startdate>20011026</startdate><enddate>20011026</enddate><creator>Denhardt, D.T.</creator><creator>Burger, E.H.</creator><creator>Kazanecki, C.</creator><creator>Krishna, S.</creator><creator>Semeins, C.M.</creator><creator>Klein-Nulend, J.</creator><general>Elsevier Inc</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>7QP</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20011026</creationdate><title>Osteopontin-Deficient Bone Cells Are Defective in Their Ability to Produce NO in Response to Pulsatile Fluid Flow</title><author>Denhardt, D.T. ; Burger, E.H. ; Kazanecki, C. ; Krishna, S. ; Semeins, C.M. ; Klein-Nulend, J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c371t-239e7687bb7ae93793e93f1e7b4f6abbaaf59ca0f505306ef1b3f9ea811e8a623</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Animals</topic><topic>Bone and Bones - cytology</topic><topic>Bone and Bones - metabolism</topic><topic>cyclooxygenase</topic><topic>cyclooxygenase 2</topic><topic>fluid flow</topic><topic>mechanotransduction</topic><topic>Mice</topic><topic>nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>osteoblast</topic><topic>osteocyte</topic><topic>Osteopontin</topic><topic>prostaglandin</topic><topic>Pulsatile Flow - physiology</topic><topic>Sialoglycoproteins - deficiency</topic><topic>Sialoglycoproteins - metabolism</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Denhardt, D.T.</creatorcontrib><creatorcontrib>Burger, E.H.</creatorcontrib><creatorcontrib>Kazanecki, C.</creatorcontrib><creatorcontrib>Krishna, S.</creatorcontrib><creatorcontrib>Semeins, C.M.</creatorcontrib><creatorcontrib>Klein-Nulend, J.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Denhardt, D.T.</au><au>Burger, E.H.</au><au>Kazanecki, C.</au><au>Krishna, S.</au><au>Semeins, C.M.</au><au>Klein-Nulend, J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Osteopontin-Deficient Bone Cells Are Defective in Their Ability to Produce NO in Response to Pulsatile Fluid Flow</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2001-10-26</date><risdate>2001</risdate><volume>288</volume><issue>2</issue><spage>448</spage><epage>453</epage><pages>448-453</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>Osteopontin (OPN) is a noncollagenous component of bone matrix. It mediates cell attachment and activates signal transduction pathways. In this work, bone cells, cultured from fragments of long bones derived from wild-type and OPN−/− (“knock-out”) mice, were exposed to pulsatile fluid flow (PFF) over a 60-min period. The medium was assayed periodically for nitric oxide (NO) and prostaglandin E2 (PGE2) release. OPN+/+ cells exhibited a peak of NO production 5–10 min after the onset of PFF, decreasing to a stable plateau at 15 min; much less NO was produced by the OPN−/− cells. PFF resulted in reduced PGE2 release by both cell types, although the reduction was less for the OPN−/− cells in the 15–30 min window. Both cell types exhibited a similar enhancement of cyclooxygenase2 mRNA levels 60 min after initiation of PFF. These results suggest that bone cells require OPN to respond fully to PFF as assessed by increased NO and reduced PGE2 synthesis.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>11606063</pmid><doi>10.1006/bbrc.2001.5780</doi><tpages>6</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0006-291X |
| ispartof | Biochemical and biophysical research communications, 2001-10, Vol.288 (2), p.448-453 |
| issn | 0006-291X 1090-2104 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_72210702 |
| source | MEDLINE; Access via ScienceDirect (Elsevier) |
| subjects | Animals Bone and Bones - cytology Bone and Bones - metabolism cyclooxygenase cyclooxygenase 2 fluid flow mechanotransduction Mice nitric oxide Nitric Oxide - metabolism osteoblast osteocyte Osteopontin prostaglandin Pulsatile Flow - physiology Sialoglycoproteins - deficiency Sialoglycoproteins - metabolism Signal Transduction |
| title | Osteopontin-Deficient Bone Cells Are Defective in Their Ability to Produce NO in Response to Pulsatile Fluid Flow |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-02T18%3A12%3A59IST&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=Osteopontin-Deficient%20Bone%20Cells%20Are%20Defective%20in%20Their%20Ability%20to%20Produce%20NO%20in%20Response%20to%20Pulsatile%20Fluid%20Flow&rft.jtitle=Biochemical%20and%20biophysical%20research%20communications&rft.au=Denhardt,%20D.T.&rft.date=2001-10-26&rft.volume=288&rft.issue=2&rft.spage=448&rft.epage=453&rft.pages=448-453&rft.issn=0006-291X&rft.eissn=1090-2104&rft_id=info:doi/10.1006/bbrc.2001.5780&rft_dat=%3Cproquest_cross%3E18186946%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=18186946&rft_id=info:pmid/11606063&rft_els_id=S0006291X01957808&rfr_iscdi=true |