The sphingosine kinase inhibitor N,N‐dimethylsphingosine inhibits neointimal hyperplasia
Background and purpose: Sphingosine‐1‐phosphate and its receptors may be involved in vascular smooth muscle cell (VSMC) proliferation following vascular injury. Here, we evaluate the effect of d‐erythro‐N,N‐dimethylsphingosine (DMS), a sphingosine kinase (SK) inhibitor, on VSMC proliferation, apopt...
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| Veröffentlicht in: | British journal of pharmacology 2010-02, Vol.159 (3), p.543-553 |
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| description | Background and purpose: Sphingosine‐1‐phosphate and its receptors may be involved in vascular smooth muscle cell (VSMC) proliferation following vascular injury. Here, we evaluate the effect of d‐erythro‐N,N‐dimethylsphingosine (DMS), a sphingosine kinase (SK) inhibitor, on VSMC proliferation, apoptosis and neointimal formation.
Experimental approach: Growth responses in vitro to fetal calf serum (FCS) were measured by [3H]‐thymidine incorporation and extracellular signal‐regulated kinase‐1/2 (ERK‐1/2) activation in quiescent primary cultures of porcine VSMC in the presence and absence of various concentrations of the SK inhibitor DMS. In vivo treatment with DMS was delivered with a local endoluminal catheter, following balloon injury of coronary arteries. The artery intimal formation was investigated by angiography, myography and histomorphometry.
Key results: In vitro experiments indicated that DMS induced a dose‐dependent reduction in [3H]‐thymidine incorporation and ERK‐1/2 activation via a protein kinase C (PKC) independent mechanism with an IC50 value of 12 ± 6 and 15 ± 10 µM respectively. DMS also reduced Akt signalling. Four weeks following in vivo delivery of DMS, complete functional endothelial regeneration was observed in all treatment groups, with significant reduction of intimal formation (vehicle 23.7 ± 4.6% vs. DMS infusion 8.92 ± 2.9%, P |
| doi_str_mv | 10.1111/j.1476-5381.2009.00533.x |
| format | Article |
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Experimental approach: Growth responses in vitro to fetal calf serum (FCS) were measured by [3H]‐thymidine incorporation and extracellular signal‐regulated kinase‐1/2 (ERK‐1/2) activation in quiescent primary cultures of porcine VSMC in the presence and absence of various concentrations of the SK inhibitor DMS. In vivo treatment with DMS was delivered with a local endoluminal catheter, following balloon injury of coronary arteries. The artery intimal formation was investigated by angiography, myography and histomorphometry.
Key results: In vitro experiments indicated that DMS induced a dose‐dependent reduction in [3H]‐thymidine incorporation and ERK‐1/2 activation via a protein kinase C (PKC) independent mechanism with an IC50 value of 12 ± 6 and 15 ± 10 µM respectively. DMS also reduced Akt signalling. Four weeks following in vivo delivery of DMS, complete functional endothelial regeneration was observed in all treatment groups, with significant reduction of intimal formation (vehicle 23.7 ± 4.6% vs. DMS infusion 8.92 ± 2.9%, P < 0.05).
Conclusions and implications: Taken together, these results demonstrate that local administration of the SK inhibitor, DMS, reduced neointimal formation, and this effect could involve inhibition of ERK‐1/2 and Akt signalling, and modulation of smooth muscle growth.</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1111/j.1476-5381.2009.00533.x</identifier><identifier>PMID: 20015089</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; anti‐proliferative ; Apoptosis - drug effects ; Biological and medical sciences ; Catheterization ; Cell Proliferation - drug effects ; extracellular signal‐regulated protein kinase ; Hyperplasia - pathology ; intimal thickening ; Lysophospholipids ; Male ; Medical sciences ; Mitogen-Activated Protein Kinase 3 - metabolism ; Mitogen-Activated Protein Kinase 3 - pharmacology ; Muscle, Smooth, Vascular - cytology ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - pathology ; Myocytes, Smooth Muscle - metabolism ; Pharmacology. Drug treatments ; Phosphotransferases (Alcohol Group Acceptor) ; protein kinase C ; Protein Kinase C - metabolism ; Protein Kinase C - pharmacology ; Protein Kinase Inhibitors - pharmacology ; Proto-Oncogene Proteins c-akt - metabolism ; Research Papers ; restenosis ; Signal Transduction - drug effects ; smooth muscle cells (vascular) ; sphingosine ; Sphingosine - analogs & derivatives ; Sphingosine - pharmacology ; sphingosine kinase ; Sus scrofa ; Tunica Intima - drug effects ; Tunica Intima - metabolism ; Tunica Intima - pathology</subject><ispartof>British journal of pharmacology, 2010-02, Vol.159 (3), p.543-553</ispartof><rights>2009 The Authors. Journal compilation © 2009 The British Pharmacological Society</rights><rights>2015 INIST-CNRS</rights><rights>Journal compilation © 2010 The British Pharmacological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5963-f7f3fab5f28f3e3fa4624501efa29d3c7bfbbc87f0536a08f5e874a9b9616b7a3</citedby><cites>FETCH-LOGICAL-c5963-f7f3fab5f28f3e3fa4624501efa29d3c7bfbbc87f0536a08f5e874a9b9616b7a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2828019/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2828019/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,1427,27901,27902,45550,45551,46384,46808,53766,53768</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22415124$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20015089$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>McDonald, Robert A</creatorcontrib><creatorcontrib>Pyne, Susan</creatorcontrib><creatorcontrib>Pyne, Nigel J</creatorcontrib><creatorcontrib>Grant, Anne</creatorcontrib><creatorcontrib>Wainwright, Cherry L</creatorcontrib><creatorcontrib>Wadsworth, Roger M</creatorcontrib><title>The sphingosine kinase inhibitor N,N‐dimethylsphingosine inhibits neointimal hyperplasia</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>Background and purpose: Sphingosine‐1‐phosphate and its receptors may be involved in vascular smooth muscle cell (VSMC) proliferation following vascular injury. Here, we evaluate the effect of d‐erythro‐N,N‐dimethylsphingosine (DMS), a sphingosine kinase (SK) inhibitor, on VSMC proliferation, apoptosis and neointimal formation.
Experimental approach: Growth responses in vitro to fetal calf serum (FCS) were measured by [3H]‐thymidine incorporation and extracellular signal‐regulated kinase‐1/2 (ERK‐1/2) activation in quiescent primary cultures of porcine VSMC in the presence and absence of various concentrations of the SK inhibitor DMS. In vivo treatment with DMS was delivered with a local endoluminal catheter, following balloon injury of coronary arteries. The artery intimal formation was investigated by angiography, myography and histomorphometry.
Key results: In vitro experiments indicated that DMS induced a dose‐dependent reduction in [3H]‐thymidine incorporation and ERK‐1/2 activation via a protein kinase C (PKC) independent mechanism with an IC50 value of 12 ± 6 and 15 ± 10 µM respectively. DMS also reduced Akt signalling. Four weeks following in vivo delivery of DMS, complete functional endothelial regeneration was observed in all treatment groups, with significant reduction of intimal formation (vehicle 23.7 ± 4.6% vs. DMS infusion 8.92 ± 2.9%, P < 0.05).
Conclusions and implications: Taken together, these results demonstrate that local administration of the SK inhibitor, DMS, reduced neointimal formation, and this effect could involve inhibition of ERK‐1/2 and Akt signalling, and modulation of smooth muscle growth.</description><subject>Animals</subject><subject>anti‐proliferative</subject><subject>Apoptosis - drug effects</subject><subject>Biological and medical sciences</subject><subject>Catheterization</subject><subject>Cell Proliferation - drug effects</subject><subject>extracellular signal‐regulated protein kinase</subject><subject>Hyperplasia - pathology</subject><subject>intimal thickening</subject><subject>Lysophospholipids</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mitogen-Activated Protein Kinase 3 - metabolism</subject><subject>Mitogen-Activated Protein Kinase 3 - pharmacology</subject><subject>Muscle, Smooth, Vascular - cytology</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Muscle, Smooth, Vascular - pathology</subject><subject>Myocytes, Smooth Muscle - metabolism</subject><subject>Pharmacology. Drug treatments</subject><subject>Phosphotransferases (Alcohol Group Acceptor)</subject><subject>protein kinase C</subject><subject>Protein Kinase C - metabolism</subject><subject>Protein Kinase C - pharmacology</subject><subject>Protein Kinase Inhibitors - pharmacology</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Research Papers</subject><subject>restenosis</subject><subject>Signal Transduction - drug effects</subject><subject>smooth muscle cells (vascular)</subject><subject>sphingosine</subject><subject>Sphingosine - analogs & derivatives</subject><subject>Sphingosine - pharmacology</subject><subject>sphingosine kinase</subject><subject>Sus scrofa</subject><subject>Tunica Intima - drug effects</subject><subject>Tunica Intima - metabolism</subject><subject>Tunica Intima - pathology</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkcFu1DAURa0K1A6lv1BFQogNSZ_tOHYkVKlUQJGqwqJs2FhOxm48eJzUzkBnxyfwjXwJDjMdCiu88ZPeuVfv6iKUYShweieLApe8yhkVuCAAdQHAKC3u9tBst3iEZgDAc4yFOEBPYlwApCVn--ggaTADUc_Q5-tOZ3HorL_po_U6-2K9ijqzvrONHfuQXb28-vn9x9wu9dit3UN0y8TM69760S6Vy7r1oMPgVLTqKXpslIv6aPsfok9v31yfX-SXH969Pz-7zFtWVzQ33FCjGmaIMFSnsaxIyQBro0g9py1vTNO0gpsUsVIgDNOCl6pu6gpXDVf0EJ1ufIdVs9TzVvsxKCeHkA4Ka9krK__eeNvJm_6rJIIIwHUyeLE1CP3tSsdRLm1stXMqBVtFySkVHKCayGf_kIt-FXxKJzErGceCQJUosaHa0McYtNndgkFO_cmFnGqSU01y6k_-7k_eJenxwyw74X1hCXi-BVRslTNB-dbGPxwpMcOkTNyrDffNOr3-7wPk648XaaC_APRAuYw</recordid><startdate>201002</startdate><enddate>201002</enddate><creator>McDonald, Robert A</creator><creator>Pyne, Susan</creator><creator>Pyne, Nigel J</creator><creator>Grant, Anne</creator><creator>Wainwright, Cherry L</creator><creator>Wadsworth, Roger M</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing Group</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>7QP</scope><scope>7TK</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201002</creationdate><title>The sphingosine kinase inhibitor N,N‐dimethylsphingosine inhibits neointimal hyperplasia</title><author>McDonald, Robert A ; Pyne, Susan ; Pyne, Nigel J ; Grant, Anne ; Wainwright, Cherry L ; Wadsworth, Roger M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5963-f7f3fab5f28f3e3fa4624501efa29d3c7bfbbc87f0536a08f5e874a9b9616b7a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Animals</topic><topic>anti‐proliferative</topic><topic>Apoptosis - drug effects</topic><topic>Biological and medical sciences</topic><topic>Catheterization</topic><topic>Cell Proliferation - drug effects</topic><topic>extracellular signal‐regulated protein kinase</topic><topic>Hyperplasia - pathology</topic><topic>intimal thickening</topic><topic>Lysophospholipids</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mitogen-Activated Protein Kinase 3 - metabolism</topic><topic>Mitogen-Activated Protein Kinase 3 - pharmacology</topic><topic>Muscle, Smooth, Vascular - cytology</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Muscle, Smooth, Vascular - pathology</topic><topic>Myocytes, Smooth Muscle - metabolism</topic><topic>Pharmacology. Drug treatments</topic><topic>Phosphotransferases (Alcohol Group Acceptor)</topic><topic>protein kinase C</topic><topic>Protein Kinase C - metabolism</topic><topic>Protein Kinase C - pharmacology</topic><topic>Protein Kinase Inhibitors - pharmacology</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Research Papers</topic><topic>restenosis</topic><topic>Signal Transduction - drug effects</topic><topic>smooth muscle cells (vascular)</topic><topic>sphingosine</topic><topic>Sphingosine - analogs & derivatives</topic><topic>Sphingosine - pharmacology</topic><topic>sphingosine kinase</topic><topic>Sus scrofa</topic><topic>Tunica Intima - drug effects</topic><topic>Tunica Intima - metabolism</topic><topic>Tunica Intima - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>McDonald, Robert A</creatorcontrib><creatorcontrib>Pyne, Susan</creatorcontrib><creatorcontrib>Pyne, Nigel J</creatorcontrib><creatorcontrib>Grant, Anne</creatorcontrib><creatorcontrib>Wainwright, Cherry L</creatorcontrib><creatorcontrib>Wadsworth, Roger M</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>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>McDonald, Robert A</au><au>Pyne, Susan</au><au>Pyne, Nigel J</au><au>Grant, Anne</au><au>Wainwright, Cherry L</au><au>Wadsworth, Roger M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The sphingosine kinase inhibitor N,N‐dimethylsphingosine inhibits neointimal hyperplasia</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2010-02</date><risdate>2010</risdate><volume>159</volume><issue>3</issue><spage>543</spage><epage>553</epage><pages>543-553</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>Background and purpose: Sphingosine‐1‐phosphate and its receptors may be involved in vascular smooth muscle cell (VSMC) proliferation following vascular injury. Here, we evaluate the effect of d‐erythro‐N,N‐dimethylsphingosine (DMS), a sphingosine kinase (SK) inhibitor, on VSMC proliferation, apoptosis and neointimal formation.
Experimental approach: Growth responses in vitro to fetal calf serum (FCS) were measured by [3H]‐thymidine incorporation and extracellular signal‐regulated kinase‐1/2 (ERK‐1/2) activation in quiescent primary cultures of porcine VSMC in the presence and absence of various concentrations of the SK inhibitor DMS. In vivo treatment with DMS was delivered with a local endoluminal catheter, following balloon injury of coronary arteries. The artery intimal formation was investigated by angiography, myography and histomorphometry.
Key results: In vitro experiments indicated that DMS induced a dose‐dependent reduction in [3H]‐thymidine incorporation and ERK‐1/2 activation via a protein kinase C (PKC) independent mechanism with an IC50 value of 12 ± 6 and 15 ± 10 µM respectively. DMS also reduced Akt signalling. Four weeks following in vivo delivery of DMS, complete functional endothelial regeneration was observed in all treatment groups, with significant reduction of intimal formation (vehicle 23.7 ± 4.6% vs. DMS infusion 8.92 ± 2.9%, P < 0.05).
Conclusions and implications: Taken together, these results demonstrate that local administration of the SK inhibitor, DMS, reduced neointimal formation, and this effect could involve inhibition of ERK‐1/2 and Akt signalling, and modulation of smooth muscle growth.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>20015089</pmid><doi>10.1111/j.1476-5381.2009.00533.x</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals anti‐proliferative Apoptosis - drug effects Biological and medical sciences Catheterization Cell Proliferation - drug effects extracellular signal‐regulated protein kinase Hyperplasia - pathology intimal thickening Lysophospholipids Male Medical sciences Mitogen-Activated Protein Kinase 3 - metabolism Mitogen-Activated Protein Kinase 3 - pharmacology Muscle, Smooth, Vascular - cytology Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - pathology Myocytes, Smooth Muscle - metabolism Pharmacology. Drug treatments Phosphotransferases (Alcohol Group Acceptor) protein kinase C Protein Kinase C - metabolism Protein Kinase C - pharmacology Protein Kinase Inhibitors - pharmacology Proto-Oncogene Proteins c-akt - metabolism Research Papers restenosis Signal Transduction - drug effects smooth muscle cells (vascular) sphingosine Sphingosine - analogs & derivatives Sphingosine - pharmacology sphingosine kinase Sus scrofa Tunica Intima - drug effects Tunica Intima - metabolism Tunica Intima - pathology |
| title | The sphingosine kinase inhibitor N,N‐dimethylsphingosine inhibits neointimal hyperplasia |
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