Atorvastatin reduces platelet-oxidized-LDL receptor expression in hypercholesterolaemic patients
Background Oxidized‐LDL (ox‐LDL) are proatherogenic and platelet‐activating molecules. Atorvastatin reduces platelet activity before cholesterol‐lowering action. CD36 and lectin‐like oxidized‐LDL receptor‐1 (LOX‐1) are specific ox‐LDL receptors expressed also in platelets. This study was planned to...
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| Veröffentlicht in: | European journal of clinical investigation 2005-01, Vol.35 (1), p.47-51 |
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| creator | Puccetti, L. Sawamura, T. Pasqui, A. L. Pastorelli, M. Auteri, A. Bruni, F. |
| description | Background Oxidized‐LDL (ox‐LDL) are proatherogenic and platelet‐activating molecules. Atorvastatin reduces platelet activity before cholesterol‐lowering action. CD36 and lectin‐like oxidized‐LDL receptor‐1 (LOX‐1) are specific ox‐LDL receptors expressed also in platelets. This study was planned to address whether the possible rapid effect of atorvastatin on platelets could be related to modulation of ox‐LDL receptors.
Materials and methods Forty‐eight hypercholesterolaemic subjects requiring statin treatment (atorvastatin 20 mg day−1) after an ineffective diet regimen were evaluated for complete lipid‐profile (chromogenic); P‐selectin (P‐sel), CD36 and LOX‐1 expression (cytofluorimetric detection); circulating and platelet‐associated ox‐LDL (ox‐ and Pox‐LDL, ELISA); and intracellular citrullin recovery (iCit, HPLC) at baseline and 3, 6 and 9 days after inclusion in the study. Moreover, we studied 48 normal controls matched for sex and age.
Results Platelet activity expressed by P‐sel (in resting and thrombin‐activated cells), CD36 and LOX‐1 were increased in hypercholesterolaemic subjects (all P |
| doi_str_mv | 10.1111/j.1365-2362.2005.01446.x |
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Materials and methods Forty‐eight hypercholesterolaemic subjects requiring statin treatment (atorvastatin 20 mg day−1) after an ineffective diet regimen were evaluated for complete lipid‐profile (chromogenic); P‐selectin (P‐sel), CD36 and LOX‐1 expression (cytofluorimetric detection); circulating and platelet‐associated ox‐LDL (ox‐ and Pox‐LDL, ELISA); and intracellular citrullin recovery (iCit, HPLC) at baseline and 3, 6 and 9 days after inclusion in the study. Moreover, we studied 48 normal controls matched for sex and age.
Results Platelet activity expressed by P‐sel (in resting and thrombin‐activated cells), CD36 and LOX‐1 were increased in hypercholesterolaemic subjects (all P < 0·01). Atorvastatin induced a reduction of CD36 at 6 days (P < 0·05); and P‐sel in resting (P < 0·001) and activated cells (P < 0·001) and LOX‐1 were reduced at 9 days (all P < 0·001) in association with decreased Pox‐LDL (P < 0·001) and increased iCit (P < 0·01). All data were obtained before a significant reduction of LDL and ox‐LDL was achieved (P = 0·109 and 0·113).
Discussion Present data suggest that platelet deactivation by atorvastatin is related to CD36 and LOX‐1 expression reduction before significant LDL changes. Moreover, the modulation of LOX‐1 can be considered a self‐relevant antiatherothrombotic action of atoravastin owing to the important role of this receptor in the ox‐LDL‐mediated vascular damage.]]></description><identifier>ISSN: 0014-2972</identifier><identifier>EISSN: 1365-2362</identifier><identifier>DOI: 10.1111/j.1365-2362.2005.01446.x</identifier><identifier>PMID: 15638819</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Adult ; Analysis of Variance ; Anticholesteremic Agents - therapeutic use ; Atherothrombosis ; atorvastatin ; Atorvastatin Calcium ; Biological and medical sciences ; Blood Platelets - drug effects ; Blood Platelets - metabolism ; CD36 ; CD36 Antigens - blood ; Citrulline - metabolism ; Female ; Flow Cytometry ; General aspects ; Heptanoic Acids - therapeutic use ; Humans ; Hypercholesterolemia - drug therapy ; Hypercholesterolemia - metabolism ; Lipoproteins, LDL - blood ; LOX-1 ; Male ; Medical sciences ; Middle Aged ; Nitric Oxide Synthase - metabolism ; ox-LDL ; P-Selectin - blood ; Platelet Activation ; Pyrroles - therapeutic use ; Receptors, LDL - blood ; Receptors, LDL - metabolism ; Receptors, Oxidized LDL ; Scavenger Receptors, Class E</subject><ispartof>European journal of clinical investigation, 2005-01, Vol.35 (1), p.47-51</ispartof><rights>2005 INIST-CNRS</rights><rights>Copyright Blackwell Publishing Jan 2005</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4626-35db4ae8aeaa992b9ed823b6b05ff792072198aeff6426fd82cfeaff7777c7033</citedby><cites>FETCH-LOGICAL-c4626-35db4ae8aeaa992b9ed823b6b05ff792072198aeff6426fd82cfeaff7777c7033</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1365-2362.2005.01446.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1365-2362.2005.01446.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1416,4022,27922,27923,27924,45573,45574</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16468085$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15638819$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Puccetti, L.</creatorcontrib><creatorcontrib>Sawamura, T.</creatorcontrib><creatorcontrib>Pasqui, A. L.</creatorcontrib><creatorcontrib>Pastorelli, M.</creatorcontrib><creatorcontrib>Auteri, A.</creatorcontrib><creatorcontrib>Bruni, F.</creatorcontrib><title>Atorvastatin reduces platelet-oxidized-LDL receptor expression in hypercholesterolaemic patients</title><title>European journal of clinical investigation</title><addtitle>Eur J Clin Invest</addtitle><description><![CDATA[Background Oxidized‐LDL (ox‐LDL) are proatherogenic and platelet‐activating molecules. Atorvastatin reduces platelet activity before cholesterol‐lowering action. CD36 and lectin‐like oxidized‐LDL receptor‐1 (LOX‐1) are specific ox‐LDL receptors expressed also in platelets. This study was planned to address whether the possible rapid effect of atorvastatin on platelets could be related to modulation of ox‐LDL receptors.
Materials and methods Forty‐eight hypercholesterolaemic subjects requiring statin treatment (atorvastatin 20 mg day−1) after an ineffective diet regimen were evaluated for complete lipid‐profile (chromogenic); P‐selectin (P‐sel), CD36 and LOX‐1 expression (cytofluorimetric detection); circulating and platelet‐associated ox‐LDL (ox‐ and Pox‐LDL, ELISA); and intracellular citrullin recovery (iCit, HPLC) at baseline and 3, 6 and 9 days after inclusion in the study. Moreover, we studied 48 normal controls matched for sex and age.
Results Platelet activity expressed by P‐sel (in resting and thrombin‐activated cells), CD36 and LOX‐1 were increased in hypercholesterolaemic subjects (all P < 0·01). Atorvastatin induced a reduction of CD36 at 6 days (P < 0·05); and P‐sel in resting (P < 0·001) and activated cells (P < 0·001) and LOX‐1 were reduced at 9 days (all P < 0·001) in association with decreased Pox‐LDL (P < 0·001) and increased iCit (P < 0·01). All data were obtained before a significant reduction of LDL and ox‐LDL was achieved (P = 0·109 and 0·113).
Discussion Present data suggest that platelet deactivation by atorvastatin is related to CD36 and LOX‐1 expression reduction before significant LDL changes. Moreover, the modulation of LOX‐1 can be considered a self‐relevant antiatherothrombotic action of atoravastin owing to the important role of this receptor in the ox‐LDL‐mediated vascular damage.]]></description><subject>Adult</subject><subject>Analysis of Variance</subject><subject>Anticholesteremic Agents - therapeutic use</subject><subject>Atherothrombosis</subject><subject>atorvastatin</subject><subject>Atorvastatin Calcium</subject><subject>Biological and medical sciences</subject><subject>Blood Platelets - drug effects</subject><subject>Blood Platelets - metabolism</subject><subject>CD36</subject><subject>CD36 Antigens - blood</subject><subject>Citrulline - metabolism</subject><subject>Female</subject><subject>Flow Cytometry</subject><subject>General aspects</subject><subject>Heptanoic Acids - therapeutic use</subject><subject>Humans</subject><subject>Hypercholesterolemia - drug therapy</subject><subject>Hypercholesterolemia - metabolism</subject><subject>Lipoproteins, LDL - blood</subject><subject>LOX-1</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>ox-LDL</subject><subject>P-Selectin - blood</subject><subject>Platelet Activation</subject><subject>Pyrroles - therapeutic use</subject><subject>Receptors, LDL - blood</subject><subject>Receptors, LDL - metabolism</subject><subject>Receptors, Oxidized LDL</subject><subject>Scavenger Receptors, Class E</subject><issn>0014-2972</issn><issn>1365-2362</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc1u1DAUhS0EosPAK6AIie4S_BfHWbCopqUURbABsTSOc6N6yCTBzkCmT98bZtRKrPDGls93jq7uISRhNGN43m0zJlSecqF4xinNM8qkVNn8hKwehKdkRfE75WXBz8iLGLeUUs0Ef07OWK6E1qxckR8X0xB-2zjZyfdJgGbvICZjZyfoYEqH2Tf-Dpq0uqxQdTAinsA8BojRD32CptvDCMHdDh3ECcLQWdh5l4wYCP0UX5Jnre0ivDrda_Ltw9XXzce0-nJ9s7moUicVV6nIm1pa0BasLUtel9BoLmpV07xti5LTgrMS1bZVkqsWRdeCRQmPK6gQa3J-zB3D8GuPo5idjw66zvYw7KNRhZC5lgrBN_-A22EfepzNsLJkXGmMWxN9hFwYYgzQmjH4nQ0Hw6hZKjBbs2zaLJs2SwXmbwVmRuvrU_6-3kHzaDztHIG3J8BGZ7s22N75-MgpqTTVOXLvj9wf38HhvwcwV5ub5YX-9Oj32Mv84Lfh57KMIjffP1-b6lLSSspPphL3-Xmypw</recordid><startdate>200501</startdate><enddate>200501</enddate><creator>Puccetti, L.</creator><creator>Sawamura, T.</creator><creator>Pasqui, A. L.</creator><creator>Pastorelli, M.</creator><creator>Auteri, A.</creator><creator>Bruni, F.</creator><general>Blackwell Science Ltd</general><general>Blackwell</general><general>Blackwell Publishing Ltd</general><scope>BSCLL</scope><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>7QO</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>200501</creationdate><title>Atorvastatin reduces platelet-oxidized-LDL receptor expression in hypercholesterolaemic patients</title><author>Puccetti, L. ; Sawamura, T. ; Pasqui, A. L. ; Pastorelli, M. ; Auteri, A. ; Bruni, F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4626-35db4ae8aeaa992b9ed823b6b05ff792072198aeff6426fd82cfeaff7777c7033</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adult</topic><topic>Analysis of Variance</topic><topic>Anticholesteremic Agents - therapeutic use</topic><topic>Atherothrombosis</topic><topic>atorvastatin</topic><topic>Atorvastatin Calcium</topic><topic>Biological and medical sciences</topic><topic>Blood Platelets - drug effects</topic><topic>Blood Platelets - metabolism</topic><topic>CD36</topic><topic>CD36 Antigens - blood</topic><topic>Citrulline - metabolism</topic><topic>Female</topic><topic>Flow Cytometry</topic><topic>General aspects</topic><topic>Heptanoic Acids - therapeutic use</topic><topic>Humans</topic><topic>Hypercholesterolemia - drug therapy</topic><topic>Hypercholesterolemia - metabolism</topic><topic>Lipoproteins, LDL - blood</topic><topic>LOX-1</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>ox-LDL</topic><topic>P-Selectin - blood</topic><topic>Platelet Activation</topic><topic>Pyrroles - therapeutic use</topic><topic>Receptors, LDL - blood</topic><topic>Receptors, LDL - metabolism</topic><topic>Receptors, Oxidized LDL</topic><topic>Scavenger Receptors, Class E</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Puccetti, L.</creatorcontrib><creatorcontrib>Sawamura, T.</creatorcontrib><creatorcontrib>Pasqui, A. L.</creatorcontrib><creatorcontrib>Pastorelli, M.</creatorcontrib><creatorcontrib>Auteri, A.</creatorcontrib><creatorcontrib>Bruni, F.</creatorcontrib><collection>Istex</collection><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>Biotechnology Research Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of clinical investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Puccetti, L.</au><au>Sawamura, T.</au><au>Pasqui, A. L.</au><au>Pastorelli, M.</au><au>Auteri, A.</au><au>Bruni, F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Atorvastatin reduces platelet-oxidized-LDL receptor expression in hypercholesterolaemic patients</atitle><jtitle>European journal of clinical investigation</jtitle><addtitle>Eur J Clin Invest</addtitle><date>2005-01</date><risdate>2005</risdate><volume>35</volume><issue>1</issue><spage>47</spage><epage>51</epage><pages>47-51</pages><issn>0014-2972</issn><eissn>1365-2362</eissn><abstract><![CDATA[Background Oxidized‐LDL (ox‐LDL) are proatherogenic and platelet‐activating molecules. Atorvastatin reduces platelet activity before cholesterol‐lowering action. CD36 and lectin‐like oxidized‐LDL receptor‐1 (LOX‐1) are specific ox‐LDL receptors expressed also in platelets. This study was planned to address whether the possible rapid effect of atorvastatin on platelets could be related to modulation of ox‐LDL receptors.
Materials and methods Forty‐eight hypercholesterolaemic subjects requiring statin treatment (atorvastatin 20 mg day−1) after an ineffective diet regimen were evaluated for complete lipid‐profile (chromogenic); P‐selectin (P‐sel), CD36 and LOX‐1 expression (cytofluorimetric detection); circulating and platelet‐associated ox‐LDL (ox‐ and Pox‐LDL, ELISA); and intracellular citrullin recovery (iCit, HPLC) at baseline and 3, 6 and 9 days after inclusion in the study. Moreover, we studied 48 normal controls matched for sex and age.
Results Platelet activity expressed by P‐sel (in resting and thrombin‐activated cells), CD36 and LOX‐1 were increased in hypercholesterolaemic subjects (all P < 0·01). Atorvastatin induced a reduction of CD36 at 6 days (P < 0·05); and P‐sel in resting (P < 0·001) and activated cells (P < 0·001) and LOX‐1 were reduced at 9 days (all P < 0·001) in association with decreased Pox‐LDL (P < 0·001) and increased iCit (P < 0·01). All data were obtained before a significant reduction of LDL and ox‐LDL was achieved (P = 0·109 and 0·113).
Discussion Present data suggest that platelet deactivation by atorvastatin is related to CD36 and LOX‐1 expression reduction before significant LDL changes. Moreover, the modulation of LOX‐1 can be considered a self‐relevant antiatherothrombotic action of atoravastin owing to the important role of this receptor in the ox‐LDL‐mediated vascular damage.]]></abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>15638819</pmid><doi>10.1111/j.1365-2362.2005.01446.x</doi><tpages>5</tpages></addata></record> |
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| subjects | Adult Analysis of Variance Anticholesteremic Agents - therapeutic use Atherothrombosis atorvastatin Atorvastatin Calcium Biological and medical sciences Blood Platelets - drug effects Blood Platelets - metabolism CD36 CD36 Antigens - blood Citrulline - metabolism Female Flow Cytometry General aspects Heptanoic Acids - therapeutic use Humans Hypercholesterolemia - drug therapy Hypercholesterolemia - metabolism Lipoproteins, LDL - blood LOX-1 Male Medical sciences Middle Aged Nitric Oxide Synthase - metabolism ox-LDL P-Selectin - blood Platelet Activation Pyrroles - therapeutic use Receptors, LDL - blood Receptors, LDL - metabolism Receptors, Oxidized LDL Scavenger Receptors, Class E |
| title | Atorvastatin reduces platelet-oxidized-LDL receptor expression in hypercholesterolaemic patients |
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