High density lipoproteins downregulate basic fibroblast growth factor production and release in minimally oxidated-LDL treated smooth muscle cells
Increase in plasma low density lipoprotein (LDL) levels and/or decrease in high density lipoprotein (HDL) levels are major risk factors for the development of atherosclerosis. An oxidative modification of LDL represents a key process in atherogenesis. It is well known that the LDL/HDL ratio is more...
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| Veröffentlicht in: | Atherosclerosis 2006-12, Vol.189 (2), p.303-309 |
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| creator | Cucina, Alessandra Scavo, Maria-Principia Muzzioli, Luca Coluccia, Pierpaolo Ceccarini, Simone Fuso, Andrea Cavallaro, Antonino |
| description | Increase in plasma low density lipoprotein (LDL) levels and/or decrease in high density lipoprotein (HDL) levels are major risk factors for the development of atherosclerosis. An oxidative modification of LDL represents a key process in atherogenesis. It is well known that the LDL/HDL ratio is more important than the individual LDL and HDL levels to predict atherosclerosis. The purpose of our study was to investigate the effects of mildly oxidized LDL (minimally modified LDL: MM-LDL) and HDL, administrated alone or in combination, on the production and release of basic fibroblast growth factor (bFGF) by bovine aortic smooth muscle cells (SMCs) in culture. MM-LDL and HDL have opposite effects on aortic SMCs: MM-LDL increases both bFGF production and release and SMC proliferation, while HDL decreases both bFGF production and release and SMC proliferation. The effects of either MM-LDL or HDL on SMCs are mediated through a Gi-protein-coupled receptor. The simultaneous treatment of SMCs with MM-LDL and HDL (MM-LDL/HDL ratio
=
4.0) produced the inhibition of MM-LDL effects. Our data suggest that the protective role of HDL could also be exerted through the inhibition of the pro-atherosclerotic effects of MM-LDL on SMCs. |
| doi_str_mv | 10.1016/j.atherosclerosis.2006.01.006 |
| format | Article |
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=
4.0) produced the inhibition of MM-LDL effects. Our data suggest that the protective role of HDL could also be exerted through the inhibition of the pro-atherosclerotic effects of MM-LDL on SMCs.</description><identifier>ISSN: 0021-9150</identifier><identifier>EISSN: 1879-1484</identifier><identifier>DOI: 10.1016/j.atherosclerosis.2006.01.006</identifier><identifier>PMID: 16490198</identifier><language>eng</language><publisher>Amsterdam: Elsevier Ireland Ltd</publisher><subject>Animals ; Aorta, Thoracic - cytology ; Aorta, Thoracic - metabolism ; Atherosclerosis ; Atherosclerosis (general aspects, experimental research) ; Atherosclerosis - etiology ; Atherosclerosis - metabolism ; Atherosclerosis - prevention & control ; bFGF ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood vessels and receptors ; Cardiology. Vascular system ; Cattle ; Cell Proliferation - drug effects ; Cells, Cultured ; Coronary heart disease ; Culture Media, Conditioned ; Down-Regulation - drug effects ; Fibroblast Growth Factor 2 - biosynthesis ; Fibroblast Growth Factor 2 - drug effects ; Fibroblast Growth Factor 2 - genetics ; Fundamental and applied biological sciences. Psychology ; HDL ; Heart ; Hormones. Endocrine system ; Lipoproteins, HDL - pharmacology ; Lipoproteins, LDL - pharmacology ; Medical sciences ; Mitosis - drug effects ; MM-LDL ; Muscle, Smooth, Vascular - cytology ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - metabolism ; Oxidation-Reduction ; Pharmacology. Drug treatments ; Polymerase Chain Reaction ; RNA, Messenger - genetics ; Smooth muscle cells ; Vertebrates: cardiovascular system</subject><ispartof>Atherosclerosis, 2006-12, Vol.189 (2), p.303-309</ispartof><rights>2006 Elsevier Ireland Ltd</rights><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c483t-80973e83729c2fa25b1298e9c7e05c80470901cb0d59a08a404590a6099be2093</citedby><cites>FETCH-LOGICAL-c483t-80973e83729c2fa25b1298e9c7e05c80470901cb0d59a08a404590a6099be2093</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0021915006000323$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18263540$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16490198$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cucina, Alessandra</creatorcontrib><creatorcontrib>Scavo, Maria-Principia</creatorcontrib><creatorcontrib>Muzzioli, Luca</creatorcontrib><creatorcontrib>Coluccia, Pierpaolo</creatorcontrib><creatorcontrib>Ceccarini, Simone</creatorcontrib><creatorcontrib>Fuso, Andrea</creatorcontrib><creatorcontrib>Cavallaro, Antonino</creatorcontrib><title>High density lipoproteins downregulate basic fibroblast growth factor production and release in minimally oxidated-LDL treated smooth muscle cells</title><title>Atherosclerosis</title><addtitle>Atherosclerosis</addtitle><description>Increase in plasma low density lipoprotein (LDL) levels and/or decrease in high density lipoprotein (HDL) levels are major risk factors for the development of atherosclerosis. An oxidative modification of LDL represents a key process in atherogenesis. It is well known that the LDL/HDL ratio is more important than the individual LDL and HDL levels to predict atherosclerosis. The purpose of our study was to investigate the effects of mildly oxidized LDL (minimally modified LDL: MM-LDL) and HDL, administrated alone or in combination, on the production and release of basic fibroblast growth factor (bFGF) by bovine aortic smooth muscle cells (SMCs) in culture. MM-LDL and HDL have opposite effects on aortic SMCs: MM-LDL increases both bFGF production and release and SMC proliferation, while HDL decreases both bFGF production and release and SMC proliferation. The effects of either MM-LDL or HDL on SMCs are mediated through a Gi-protein-coupled receptor. The simultaneous treatment of SMCs with MM-LDL and HDL (MM-LDL/HDL ratio
=
4.0) produced the inhibition of MM-LDL effects. Our data suggest that the protective role of HDL could also be exerted through the inhibition of the pro-atherosclerotic effects of MM-LDL on SMCs.</description><subject>Animals</subject><subject>Aorta, Thoracic - cytology</subject><subject>Aorta, Thoracic - metabolism</subject><subject>Atherosclerosis</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Atherosclerosis - etiology</subject><subject>Atherosclerosis - metabolism</subject><subject>Atherosclerosis - prevention & control</subject><subject>bFGF</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood vessels and receptors</subject><subject>Cardiology. Vascular system</subject><subject>Cattle</subject><subject>Cell Proliferation - drug effects</subject><subject>Cells, Cultured</subject><subject>Coronary heart disease</subject><subject>Culture Media, Conditioned</subject><subject>Down-Regulation - drug effects</subject><subject>Fibroblast Growth Factor 2 - biosynthesis</subject><subject>Fibroblast Growth Factor 2 - drug effects</subject><subject>Fibroblast Growth Factor 2 - genetics</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>HDL</subject><subject>Heart</subject><subject>Hormones. Endocrine system</subject><subject>Lipoproteins, HDL - pharmacology</subject><subject>Lipoproteins, LDL - pharmacology</subject><subject>Medical sciences</subject><subject>Mitosis - drug effects</subject><subject>MM-LDL</subject><subject>Muscle, Smooth, Vascular - cytology</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Muscle, Smooth, Vascular - metabolism</subject><subject>Oxidation-Reduction</subject><subject>Pharmacology. Drug treatments</subject><subject>Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>Smooth muscle cells</subject><subject>Vertebrates: cardiovascular system</subject><issn>0021-9150</issn><issn>1879-1484</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc9uEzEQxlcIREPhFZAv5bbLeP_aBw6o0BYpEhc4W157NnHktYPtpeQ1eOJ6lQgkTlw8Pvzmm_nmK4obChUF2r8_VDLtMfio7PqaWNUAfQW0yuVZsaFs4CVtWfu82ADUtOS0g6viVYwHAGgHyl4WV7RvOVDONsXvB7PbE40umnQi1hz9MfiExkWi_aMLuFusTEhGGY0ikxmDH62MieyCf0x7MkmVfCC5SS8qGe-IdJoEtCgjEuPIbJyZpbUn4n8ZnaV0uf20JSng-idx9j7LzMvqhyi0Nr4uXkzSRnxzqdfF97vP324fyu3X-y-3H7elalmTSgZ8aJA1Q81VPcm6G2nNGXI1IHSKZauQPaoRdMclMNlC23GQPXA-Yg28uS7enXXz8j8WjEnMJq4bSId-iaLnAA0dhgx-OIMqHzwGnMQxZE_hJCiINRRxEP-EItZQBFCRS-5_exm0jDPqv92XFDJwcwFkVNJOQTqVNf5wrO6broXM3Z85zGf5aTCIqAw6hdoEVElob_5zpSeSGre0</recordid><startdate>20061201</startdate><enddate>20061201</enddate><creator>Cucina, Alessandra</creator><creator>Scavo, Maria-Principia</creator><creator>Muzzioli, Luca</creator><creator>Coluccia, Pierpaolo</creator><creator>Ceccarini, Simone</creator><creator>Fuso, Andrea</creator><creator>Cavallaro, Antonino</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>7X8</scope></search><sort><creationdate>20061201</creationdate><title>High density lipoproteins downregulate basic fibroblast growth factor production and release in minimally oxidated-LDL treated smooth muscle cells</title><author>Cucina, Alessandra ; Scavo, Maria-Principia ; Muzzioli, Luca ; Coluccia, Pierpaolo ; Ceccarini, Simone ; Fuso, Andrea ; Cavallaro, Antonino</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c483t-80973e83729c2fa25b1298e9c7e05c80470901cb0d59a08a404590a6099be2093</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Aorta, Thoracic - cytology</topic><topic>Aorta, Thoracic - metabolism</topic><topic>Atherosclerosis</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Atherosclerosis - etiology</topic><topic>Atherosclerosis - metabolism</topic><topic>Atherosclerosis - prevention & control</topic><topic>bFGF</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood vessels and receptors</topic><topic>Cardiology. Vascular system</topic><topic>Cattle</topic><topic>Cell Proliferation - drug effects</topic><topic>Cells, Cultured</topic><topic>Coronary heart disease</topic><topic>Culture Media, Conditioned</topic><topic>Down-Regulation - drug effects</topic><topic>Fibroblast Growth Factor 2 - biosynthesis</topic><topic>Fibroblast Growth Factor 2 - drug effects</topic><topic>Fibroblast Growth Factor 2 - genetics</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>HDL</topic><topic>Heart</topic><topic>Hormones. Endocrine system</topic><topic>Lipoproteins, HDL - pharmacology</topic><topic>Lipoproteins, LDL - pharmacology</topic><topic>Medical sciences</topic><topic>Mitosis - drug effects</topic><topic>MM-LDL</topic><topic>Muscle, Smooth, Vascular - cytology</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Muscle, Smooth, Vascular - metabolism</topic><topic>Oxidation-Reduction</topic><topic>Pharmacology. Drug treatments</topic><topic>Polymerase Chain Reaction</topic><topic>RNA, Messenger - genetics</topic><topic>Smooth muscle cells</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cucina, Alessandra</creatorcontrib><creatorcontrib>Scavo, Maria-Principia</creatorcontrib><creatorcontrib>Muzzioli, Luca</creatorcontrib><creatorcontrib>Coluccia, Pierpaolo</creatorcontrib><creatorcontrib>Ceccarini, Simone</creatorcontrib><creatorcontrib>Fuso, Andrea</creatorcontrib><creatorcontrib>Cavallaro, Antonino</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>MEDLINE - Academic</collection><jtitle>Atherosclerosis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cucina, Alessandra</au><au>Scavo, Maria-Principia</au><au>Muzzioli, Luca</au><au>Coluccia, Pierpaolo</au><au>Ceccarini, Simone</au><au>Fuso, Andrea</au><au>Cavallaro, Antonino</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>High density lipoproteins downregulate basic fibroblast growth factor production and release in minimally oxidated-LDL treated smooth muscle cells</atitle><jtitle>Atherosclerosis</jtitle><addtitle>Atherosclerosis</addtitle><date>2006-12-01</date><risdate>2006</risdate><volume>189</volume><issue>2</issue><spage>303</spage><epage>309</epage><pages>303-309</pages><issn>0021-9150</issn><eissn>1879-1484</eissn><abstract>Increase in plasma low density lipoprotein (LDL) levels and/or decrease in high density lipoprotein (HDL) levels are major risk factors for the development of atherosclerosis. An oxidative modification of LDL represents a key process in atherogenesis. It is well known that the LDL/HDL ratio is more important than the individual LDL and HDL levels to predict atherosclerosis. The purpose of our study was to investigate the effects of mildly oxidized LDL (minimally modified LDL: MM-LDL) and HDL, administrated alone or in combination, on the production and release of basic fibroblast growth factor (bFGF) by bovine aortic smooth muscle cells (SMCs) in culture. MM-LDL and HDL have opposite effects on aortic SMCs: MM-LDL increases both bFGF production and release and SMC proliferation, while HDL decreases both bFGF production and release and SMC proliferation. The effects of either MM-LDL or HDL on SMCs are mediated through a Gi-protein-coupled receptor. The simultaneous treatment of SMCs with MM-LDL and HDL (MM-LDL/HDL ratio
=
4.0) produced the inhibition of MM-LDL effects. Our data suggest that the protective role of HDL could also be exerted through the inhibition of the pro-atherosclerotic effects of MM-LDL on SMCs.</abstract><cop>Amsterdam</cop><pub>Elsevier Ireland Ltd</pub><pmid>16490198</pmid><doi>10.1016/j.atherosclerosis.2006.01.006</doi><tpages>7</tpages></addata></record> |
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| ispartof | Atherosclerosis, 2006-12, Vol.189 (2), p.303-309 |
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| subjects | Animals Aorta, Thoracic - cytology Aorta, Thoracic - metabolism Atherosclerosis Atherosclerosis (general aspects, experimental research) Atherosclerosis - etiology Atherosclerosis - metabolism Atherosclerosis - prevention & control bFGF Biological and medical sciences Blood and lymphatic vessels Blood vessels and receptors Cardiology. Vascular system Cattle Cell Proliferation - drug effects Cells, Cultured Coronary heart disease Culture Media, Conditioned Down-Regulation - drug effects Fibroblast Growth Factor 2 - biosynthesis Fibroblast Growth Factor 2 - drug effects Fibroblast Growth Factor 2 - genetics Fundamental and applied biological sciences. Psychology HDL Heart Hormones. Endocrine system Lipoproteins, HDL - pharmacology Lipoproteins, LDL - pharmacology Medical sciences Mitosis - drug effects MM-LDL Muscle, Smooth, Vascular - cytology Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - metabolism Oxidation-Reduction Pharmacology. Drug treatments Polymerase Chain Reaction RNA, Messenger - genetics Smooth muscle cells Vertebrates: cardiovascular system |
| title | High density lipoproteins downregulate basic fibroblast growth factor production and release in minimally oxidated-LDL treated smooth muscle cells |
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