A validated system for simulating common carotid arterial flow in vitro: alteration of endothelial cell response
Pulsations in blood flow alter gene and protein expressions in endothelial cells (EC). A computer-controlled system was developed to mimic the common carotid artery flow waveform and shear stress levels or to provide steady flow of the same mean shear stress in a parallel plate flow chamber. The pse...
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| Veröffentlicht in: | Annals of biomedical engineering 2006-04, Vol.34 (4), p.593-604 |
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| creator | Yee, Andrew Sakurai, Yumiko Eskin, Suzanne G McIntire, Larry V |
| description | Pulsations in blood flow alter gene and protein expressions in endothelial cells (EC). A computer-controlled system was developed to mimic the common carotid artery flow waveform and shear stress levels or to provide steady flow of the same mean shear stress in a parallel plate flow chamber. The pseudo-steady state shear stress was determined from real-time pressure gradient measurements and compared to the Navier-Stokes equation solution. Following 24 h of steady flow (SF: 13 dyne/cm2), pulsatile arterial flow (AF: average = 13 dyne/cm2, range = 7-25 dyne/cm2) or static conditions, heme oxygenase-1 (HO-1) and prostaglandin H synthase-2 (PGHS-2) mRNA and protein expressions from human umbilical vein endothelial cells were measured. Relative to steady flow, pulsatile arterial flow significantly attenuated mRNA upregulation of HO-1 (SF: 7.26 +/- 2.70-fold over static, AF: 4.84 +/- 0.37-fold over static; p < 0.01) and PGHS-2 (SF: 6.11+/-1.79-fold over static, AF: 3.54+/-0.79-fold over static; p < 0.001). Pulsatile arterial flow (4.57+/-0.81-fold over static, p < 0.01) also significantly reduced the steady-flow-induced HO-1 protein upregulation (7.99 +/- 1.29-fold over static). These findings reveal that EC can discriminate between different flow patterns of the same average magnitude and respond at the molecular level. |
| doi_str_mv | 10.1007/s10439-006-9078-8 |
| format | Article |
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A computer-controlled system was developed to mimic the common carotid artery flow waveform and shear stress levels or to provide steady flow of the same mean shear stress in a parallel plate flow chamber. The pseudo-steady state shear stress was determined from real-time pressure gradient measurements and compared to the Navier-Stokes equation solution. Following 24 h of steady flow (SF: 13 dyne/cm2), pulsatile arterial flow (AF: average = 13 dyne/cm2, range = 7-25 dyne/cm2) or static conditions, heme oxygenase-1 (HO-1) and prostaglandin H synthase-2 (PGHS-2) mRNA and protein expressions from human umbilical vein endothelial cells were measured. Relative to steady flow, pulsatile arterial flow significantly attenuated mRNA upregulation of HO-1 (SF: 7.26 +/- 2.70-fold over static, AF: 4.84 +/- 0.37-fold over static; p < 0.01) and PGHS-2 (SF: 6.11+/-1.79-fold over static, AF: 3.54+/-0.79-fold over static; p < 0.001). Pulsatile arterial flow (4.57+/-0.81-fold over static, p < 0.01) also significantly reduced the steady-flow-induced HO-1 protein upregulation (7.99 +/- 1.29-fold over static). These findings reveal that EC can discriminate between different flow patterns of the same average magnitude and respond at the molecular level.</description><identifier>ISSN: 0090-6964</identifier><identifier>EISSN: 1573-9686</identifier><identifier>DOI: 10.1007/s10439-006-9078-8</identifier><identifier>PMID: 16565786</identifier><language>eng</language><publisher>United States: Springer Nature B.V</publisher><subject>Blood vessels ; Carotid Artery, Common - physiology ; Cells ; Cells, Cultured ; Computer Simulation ; Cyclooxygenase 2 - biosynthesis ; Endothelial Cells - cytology ; Endothelial Cells - enzymology ; Gene Expression Regulation, Enzymologic - physiology ; Heme Oxygenase-1 - biosynthesis ; Models, Cardiovascular ; Shear stress ; Stress ; Stress, Mechanical</subject><ispartof>Annals of biomedical engineering, 2006-04, Vol.34 (4), p.593-604</ispartof><rights>Springer Science+Business Media, Inc. 2006</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c420t-6c3024cb0848b589cbb22884bb1f4c6ae05cbfa7106cd70a13ad31b79cb5eafd3</citedby><cites>FETCH-LOGICAL-c420t-6c3024cb0848b589cbb22884bb1f4c6ae05cbfa7106cd70a13ad31b79cb5eafd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16565786$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yee, Andrew</creatorcontrib><creatorcontrib>Sakurai, Yumiko</creatorcontrib><creatorcontrib>Eskin, Suzanne G</creatorcontrib><creatorcontrib>McIntire, Larry V</creatorcontrib><title>A validated system for simulating common carotid arterial flow in vitro: alteration of endothelial cell response</title><title>Annals of biomedical engineering</title><addtitle>Ann Biomed Eng</addtitle><description>Pulsations in blood flow alter gene and protein expressions in endothelial cells (EC). A computer-controlled system was developed to mimic the common carotid artery flow waveform and shear stress levels or to provide steady flow of the same mean shear stress in a parallel plate flow chamber. The pseudo-steady state shear stress was determined from real-time pressure gradient measurements and compared to the Navier-Stokes equation solution. Following 24 h of steady flow (SF: 13 dyne/cm2), pulsatile arterial flow (AF: average = 13 dyne/cm2, range = 7-25 dyne/cm2) or static conditions, heme oxygenase-1 (HO-1) and prostaglandin H synthase-2 (PGHS-2) mRNA and protein expressions from human umbilical vein endothelial cells were measured. Relative to steady flow, pulsatile arterial flow significantly attenuated mRNA upregulation of HO-1 (SF: 7.26 +/- 2.70-fold over static, AF: 4.84 +/- 0.37-fold over static; p < 0.01) and PGHS-2 (SF: 6.11+/-1.79-fold over static, AF: 3.54+/-0.79-fold over static; p < 0.001). Pulsatile arterial flow (4.57+/-0.81-fold over static, p < 0.01) also significantly reduced the steady-flow-induced HO-1 protein upregulation (7.99 +/- 1.29-fold over static). These findings reveal that EC can discriminate between different flow patterns of the same average magnitude and respond at the molecular level.</description><subject>Blood vessels</subject><subject>Carotid Artery, Common - physiology</subject><subject>Cells</subject><subject>Cells, Cultured</subject><subject>Computer Simulation</subject><subject>Cyclooxygenase 2 - biosynthesis</subject><subject>Endothelial Cells - cytology</subject><subject>Endothelial Cells - enzymology</subject><subject>Gene Expression Regulation, Enzymologic - physiology</subject><subject>Heme Oxygenase-1 - biosynthesis</subject><subject>Models, Cardiovascular</subject><subject>Shear stress</subject><subject>Stress</subject><subject>Stress, Mechanical</subject><issn>0090-6964</issn><issn>1573-9686</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqF0k1rHSEUBmApLc1N2h_QTZEuktW0x_FzuguhXxDIJl2LOk5rcMZbdRLy7-NwLxS6aFaCPOfo0RehdwQ-EgD5qRBgdOgARDeAVJ16gXaES9oNQomXaAcwQCcGwU7QaSl3AIQoyl-jEyK44FKJHdpf4nsTw2iqH3F5LNXPeEoZlzCv0dSw_MIuzXNasDM51TBik6vPwUQ8xfSAw4LvQ83pMzax7beKRtOE_TKm-tvHDTofI86-7NNS_Bv0ajKx-LfH9Qz9_Prl9up7d33z7cfV5XXnWA-1E45Cz5wFxZTlanDW9r1SzFoyMSeMB-7sZCQB4UYJhlAzUmJlg9ybaaRn6OLQd5_Tn9WXqudQtpuYxae1aEUJkayXqsnz_0ohVTuG8WdhP3DBOOmfhWSgaiA9a_DDP_AurXlp76IlF5KqNn5D5IBcTqVkP-l9DrPJj5qA3nKgDznQLQd6y4HeZnp_bLza2Y9_K44fT58A6XqvBg</recordid><startdate>200604</startdate><enddate>200604</enddate><creator>Yee, Andrew</creator><creator>Sakurai, Yumiko</creator><creator>Eskin, Suzanne G</creator><creator>McIntire, Larry V</creator><general>Springer Nature B.V</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>3V.</scope><scope>7QF</scope><scope>7QO</scope><scope>7QQ</scope><scope>7SC</scope><scope>7SE</scope><scope>7SP</scope><scope>7SR</scope><scope>7TA</scope><scope>7TB</scope><scope>7U5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8BQ</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>F28</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H8D</scope><scope>H8G</scope><scope>HCIFZ</scope><scope>JG9</scope><scope>JQ2</scope><scope>K9.</scope><scope>KR7</scope><scope>L6V</scope><scope>L7M</scope><scope>LK8</scope><scope>L~C</scope><scope>L~D</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>M7S</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>7X8</scope></search><sort><creationdate>200604</creationdate><title>A validated system for simulating common carotid arterial flow in vitro: alteration of endothelial cell response</title><author>Yee, Andrew ; Sakurai, Yumiko ; Eskin, Suzanne G ; McIntire, Larry V</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c420t-6c3024cb0848b589cbb22884bb1f4c6ae05cbfa7106cd70a13ad31b79cb5eafd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Blood vessels</topic><topic>Carotid Artery, Common - 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Academic</collection><jtitle>Annals of biomedical engineering</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yee, Andrew</au><au>Sakurai, Yumiko</au><au>Eskin, Suzanne G</au><au>McIntire, Larry V</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A validated system for simulating common carotid arterial flow in vitro: alteration of endothelial cell response</atitle><jtitle>Annals of biomedical engineering</jtitle><addtitle>Ann Biomed Eng</addtitle><date>2006-04</date><risdate>2006</risdate><volume>34</volume><issue>4</issue><spage>593</spage><epage>604</epage><pages>593-604</pages><issn>0090-6964</issn><eissn>1573-9686</eissn><abstract>Pulsations in blood flow alter gene and protein expressions in endothelial cells (EC). A computer-controlled system was developed to mimic the common carotid artery flow waveform and shear stress levels or to provide steady flow of the same mean shear stress in a parallel plate flow chamber. The pseudo-steady state shear stress was determined from real-time pressure gradient measurements and compared to the Navier-Stokes equation solution. Following 24 h of steady flow (SF: 13 dyne/cm2), pulsatile arterial flow (AF: average = 13 dyne/cm2, range = 7-25 dyne/cm2) or static conditions, heme oxygenase-1 (HO-1) and prostaglandin H synthase-2 (PGHS-2) mRNA and protein expressions from human umbilical vein endothelial cells were measured. Relative to steady flow, pulsatile arterial flow significantly attenuated mRNA upregulation of HO-1 (SF: 7.26 +/- 2.70-fold over static, AF: 4.84 +/- 0.37-fold over static; p < 0.01) and PGHS-2 (SF: 6.11+/-1.79-fold over static, AF: 3.54+/-0.79-fold over static; p < 0.001). Pulsatile arterial flow (4.57+/-0.81-fold over static, p < 0.01) also significantly reduced the steady-flow-induced HO-1 protein upregulation (7.99 +/- 1.29-fold over static). These findings reveal that EC can discriminate between different flow patterns of the same average magnitude and respond at the molecular level.</abstract><cop>United States</cop><pub>Springer Nature B.V</pub><pmid>16565786</pmid><doi>10.1007/s10439-006-9078-8</doi><tpages>12</tpages></addata></record> |
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| subjects | Blood vessels Carotid Artery, Common - physiology Cells Cells, Cultured Computer Simulation Cyclooxygenase 2 - biosynthesis Endothelial Cells - cytology Endothelial Cells - enzymology Gene Expression Regulation, Enzymologic - physiology Heme Oxygenase-1 - biosynthesis Models, Cardiovascular Shear stress Stress Stress, Mechanical |
| title | A validated system for simulating common carotid arterial flow in vitro: alteration of endothelial cell response |
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