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Expression of Endothelial Lipase Correlates with the Size of Neointima in a Murine Model of Vascular Remodeling

Aim: Endothelial lipase (EL) regulates plasma high-density lipoprotein-cholesterol (HDL-C) levels by promoting HDL catabolism. However, it remains unknown whether the inhibition of EL has beneficial effects on the genesis of vascular diseases. Here, we investigated the role of EL on vascular remodel...

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Published in:Journal of Atherosclerosis and Thrombosis 2012, Vol.19(12), pp.1110-1127
Main Authors: Sun, Li, Ishida, Tatsuro, Okada, Takeaki, Yasuda, Tomoyuki, Hara, Tetsuya, Toh, Ryuji, Shinohara, Masakazu, Yamashita, Tomoya, Rikitake, Yoshiyuki, Hirata, Ken-ichi
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cited_by cdi_FETCH-LOGICAL-c467t-aebc32855655acf71eb8b57161f47cbb48787b4fe95be8327aec0e2ca74295f33
cites cdi_FETCH-LOGICAL-c467t-aebc32855655acf71eb8b57161f47cbb48787b4fe95be8327aec0e2ca74295f33
container_end_page 1127
container_issue 12
container_start_page 1110
container_title Journal of Atherosclerosis and Thrombosis
container_volume 19
creator Sun, Li
Ishida, Tatsuro
Okada, Takeaki
Yasuda, Tomoyuki
Hara, Tetsuya
Toh, Ryuji
Shinohara, Masakazu
Yamashita, Tomoya
Rikitake, Yoshiyuki
Hirata, Ken-ichi
description Aim: Endothelial lipase (EL) regulates plasma high-density lipoprotein-cholesterol (HDL-C) levels by promoting HDL catabolism. However, it remains unknown whether the inhibition of EL has beneficial effects on the genesis of vascular diseases. Here, we investigated the role of EL on vascular remodeling in mice. Methods: Vascular remodeling was developed by ligation of the left common carotid artery and neointimal lesions were histologically compared between EL-knockout (ELKO), EL-transgenic (ELTg), and wild-type (WT) mice. HDL was isolated from these mice, and effects of the HDL on cell growth and Erk activation were evaluated in vitro using cultured vascular smooth muscle cells. Results: Plasma HDL-C levels were 62% higher in ELKO and 13% lower in ELTg than in WT mice, after the carotid ligation. The size of neointimal lesion was significantly larger in ELTg and smaller in ELKO than in WT mice. Vascular expression of adhesion molecules was lower in ELKO and higher in ELTg compared with WT mice. Moreover, oxidative stress was attenuated in ELKO mice. HDL isolated from ELKO, ELTg, and WT mice inhibited expression of intercellular adhesion molecule-1, angiotensin II-induced activation of Erk, and growth of cultured vascular smooth muscle cells, whereas EL expression itself did not affect cell migration or growth. Conclusion: EL expression modulates vascular remodeling as well as plasma HDL-C levels. EL inactivation may increase HDL particles that can inhibit smooth muscle cell growth and migration.
doi_str_mv 10.5551/jat.13110
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However, it remains unknown whether the inhibition of EL has beneficial effects on the genesis of vascular diseases. Here, we investigated the role of EL on vascular remodeling in mice. Methods: Vascular remodeling was developed by ligation of the left common carotid artery and neointimal lesions were histologically compared between EL-knockout (ELKO), EL-transgenic (ELTg), and wild-type (WT) mice. HDL was isolated from these mice, and effects of the HDL on cell growth and Erk activation were evaluated in vitro using cultured vascular smooth muscle cells. Results: Plasma HDL-C levels were 62% higher in ELKO and 13% lower in ELTg than in WT mice, after the carotid ligation. The size of neointimal lesion was significantly larger in ELTg and smaller in ELKO than in WT mice. Vascular expression of adhesion molecules was lower in ELKO and higher in ELTg compared with WT mice. Moreover, oxidative stress was attenuated in ELKO mice. HDL isolated from ELKO, ELTg, and WT mice inhibited expression of intercellular adhesion molecule-1, angiotensin II-induced activation of Erk, and growth of cultured vascular smooth muscle cells, whereas EL expression itself did not affect cell migration or growth. Conclusion: EL expression modulates vascular remodeling as well as plasma HDL-C levels. EL inactivation may increase HDL particles that can inhibit smooth muscle cell growth and migration.</description><identifier>ISSN: 1340-3478</identifier><identifier>EISSN: 1880-3873</identifier><identifier>DOI: 10.5551/jat.13110</identifier><identifier>PMID: 22972429</identifier><language>eng</language><publisher>Japan: Japan Atherosclerosis Society</publisher><subject>Angiotensin II - metabolism ; Animals ; Carotid Artery, Common - pathology ; Cell Adhesion ; Cell Movement ; Cell Proliferation ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Endothelium, Vascular - enzymology ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Gene Expression Regulation, Enzymologic ; HDL cholesterol ; Humans ; Inflammation ; Lipase - biosynthesis ; Lipoproteins - metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myocytes, Smooth Muscle - cytology ; Neointima - pathology ; Oxidative Stress ; Proliferation ; Vascular remodeling</subject><ispartof>Journal of Atherosclerosis and Thrombosis, 2012, Vol.19(12), pp.1110-1127</ispartof><rights>2012 Japan Atherosclerosis Society</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c467t-aebc32855655acf71eb8b57161f47cbb48787b4fe95be8327aec0e2ca74295f33</citedby><cites>FETCH-LOGICAL-c467t-aebc32855655acf71eb8b57161f47cbb48787b4fe95be8327aec0e2ca74295f33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22972429$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sun, Li</creatorcontrib><creatorcontrib>Ishida, Tatsuro</creatorcontrib><creatorcontrib>Okada, Takeaki</creatorcontrib><creatorcontrib>Yasuda, Tomoyuki</creatorcontrib><creatorcontrib>Hara, Tetsuya</creatorcontrib><creatorcontrib>Toh, Ryuji</creatorcontrib><creatorcontrib>Shinohara, Masakazu</creatorcontrib><creatorcontrib>Yamashita, Tomoya</creatorcontrib><creatorcontrib>Rikitake, Yoshiyuki</creatorcontrib><creatorcontrib>Hirata, Ken-ichi</creatorcontrib><title>Expression of Endothelial Lipase Correlates with the Size of Neointima in a Murine Model of Vascular Remodeling</title><title>Journal of Atherosclerosis and Thrombosis</title><addtitle>JAT</addtitle><description>Aim: Endothelial lipase (EL) regulates plasma high-density lipoprotein-cholesterol (HDL-C) levels by promoting HDL catabolism. However, it remains unknown whether the inhibition of EL has beneficial effects on the genesis of vascular diseases. Here, we investigated the role of EL on vascular remodeling in mice. Methods: Vascular remodeling was developed by ligation of the left common carotid artery and neointimal lesions were histologically compared between EL-knockout (ELKO), EL-transgenic (ELTg), and wild-type (WT) mice. HDL was isolated from these mice, and effects of the HDL on cell growth and Erk activation were evaluated in vitro using cultured vascular smooth muscle cells. Results: Plasma HDL-C levels were 62% higher in ELKO and 13% lower in ELTg than in WT mice, after the carotid ligation. The size of neointimal lesion was significantly larger in ELTg and smaller in ELKO than in WT mice. Vascular expression of adhesion molecules was lower in ELKO and higher in ELTg compared with WT mice. Moreover, oxidative stress was attenuated in ELKO mice. HDL isolated from ELKO, ELTg, and WT mice inhibited expression of intercellular adhesion molecule-1, angiotensin II-induced activation of Erk, and growth of cultured vascular smooth muscle cells, whereas EL expression itself did not affect cell migration or growth. Conclusion: EL expression modulates vascular remodeling as well as plasma HDL-C levels. EL inactivation may increase HDL particles that can inhibit smooth muscle cell growth and migration.</description><subject>Angiotensin II - metabolism</subject><subject>Animals</subject><subject>Carotid Artery, Common - pathology</subject><subject>Cell Adhesion</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Disease Models, Animal</subject><subject>Dose-Response Relationship, Drug</subject><subject>Endothelium, Vascular - enzymology</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>Gene Expression Regulation, Enzymologic</subject><subject>HDL cholesterol</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Lipase - biosynthesis</subject><subject>Lipoproteins - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Myocytes, Smooth Muscle - cytology</subject><subject>Neointima - pathology</subject><subject>Oxidative Stress</subject><subject>Proliferation</subject><subject>Vascular remodeling</subject><issn>1340-3478</issn><issn>1880-3873</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><recordid>eNo9kEFvGjEQha0qVSG0h_6Bysf0QLK219jcGiHaRIJGSppcV7NmFozMmthepe2vjxcSLjOjeZ_eaB4hX1lxKaVkV1tIl0wwVnwgQ6Z1MRZaibM8izLPpdIDch7jtiiEkJJ_IgPOp4qXfDokfv53HzBG61vqGzpvVz5t0FlwdGH3EJHOfAjoIGGkLzZtaJbpg_2PPf4bvW2T3QG1LQW67IJtkS79Cl0vP0E0nYNA73HX72y7_kw-NuAifnnrI_L4c_5ndjNe3P26nV0vxqacqDQGrI3gWsqJlGAaxbDWtVRswppSmboutdKqLhucyhq14ArQFMgNqPyVbIQYkYuj7z745w5jqnY2GnQOWvRdrBhXomQF5z36_Yia4GMM2FT7kF8K_ypWVH2-Vc63OuSb2W9vtl29w9WJfA80Az-OwDYmWOMJgJCscXi0mubzh9p7niSzgVBhK14Bq_aNkg</recordid><startdate>20120101</startdate><enddate>20120101</enddate><creator>Sun, Li</creator><creator>Ishida, Tatsuro</creator><creator>Okada, Takeaki</creator><creator>Yasuda, Tomoyuki</creator><creator>Hara, Tetsuya</creator><creator>Toh, Ryuji</creator><creator>Shinohara, Masakazu</creator><creator>Yamashita, Tomoya</creator><creator>Rikitake, Yoshiyuki</creator><creator>Hirata, Ken-ichi</creator><general>Japan Atherosclerosis Society</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>7X8</scope></search><sort><creationdate>20120101</creationdate><title>Expression of Endothelial Lipase Correlates with the Size of Neointima in a Murine Model of Vascular Remodeling</title><author>Sun, Li ; 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HDL isolated from ELKO, ELTg, and WT mice inhibited expression of intercellular adhesion molecule-1, angiotensin II-induced activation of Erk, and growth of cultured vascular smooth muscle cells, whereas EL expression itself did not affect cell migration or growth. Conclusion: EL expression modulates vascular remodeling as well as plasma HDL-C levels. EL inactivation may increase HDL particles that can inhibit smooth muscle cell growth and migration.</abstract><cop>Japan</cop><pub>Japan Atherosclerosis Society</pub><pmid>22972429</pmid><doi>10.5551/jat.13110</doi><tpages>18</tpages><oa>free_for_read</oa></addata></record>
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ispartof Journal of Atherosclerosis and Thrombosis, 2012, Vol.19(12), pp.1110-1127
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1880-3873
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subjects Angiotensin II - metabolism
Animals
Carotid Artery, Common - pathology
Cell Adhesion
Cell Movement
Cell Proliferation
Disease Models, Animal
Dose-Response Relationship, Drug
Endothelium, Vascular - enzymology
Extracellular Signal-Regulated MAP Kinases - metabolism
Gene Expression Regulation, Enzymologic
HDL cholesterol
Humans
Inflammation
Lipase - biosynthesis
Lipoproteins - metabolism
Mice
Mice, Inbred C57BL
Mice, Knockout
Myocytes, Smooth Muscle - cytology
Neointima - pathology
Oxidative Stress
Proliferation
Vascular remodeling
title Expression of Endothelial Lipase Correlates with the Size of Neointima in a Murine Model of Vascular Remodeling
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