Enhanced External Counterpulsation Attenuates Atherosclerosis Progression Through Modulation of Proinflammatory Signal Pathway
OBJECTIVE—Shear stress may be the most crucial local factor affecting atherogenesis. The present study investigated the effect of exposure to increased shear stress promoted by enhanced external counterpulsation (EECP) on the progression of atherosclerosis and the underlying inflammation-related mol...
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| Veröffentlicht in: | Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2010-04, Vol.30 (4), p.773-780 |
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| creator | Zhang, Yan He, Xiaohong Liu, Donghong Wu, Guifu Chen, Xiaolin Ma, Hong Du, Zhimin Dong, Yugang Jin, Yafei He, Wen Wang, Kuijian Lawson, William E Hui, John C.K Zheng, Zhensheng |
| description | OBJECTIVE—Shear stress may be the most crucial local factor affecting atherogenesis. The present study investigated the effect of exposure to increased shear stress promoted by enhanced external counterpulsation (EECP) on the progression of atherosclerosis and the underlying inflammation-related molecular mechanisms in a porcine model of hypercholesterolemia.
METHODS AND RESULTS—Hypercholesterolemic pigs were subjected to a 7-week EECP intervention while being fed a high-cholesterol diet. EECP resulted in a 34.38% increase of mean wall shear stress and a significantly lower pulsatility index in the brachial artery. The animals receiving EECP showed a marked reduction in atherosclerotic lesion size in the coronary artery and abdominal aorta compared with the hypercholesterolemic control group, associated with a decrease in macrophage accumulation. The expression of a set of genes involved in inflammation (including C-reactive protein [CRP], complement 3a, vascular cell adhesion molecule-1 [VCAM-1], and inducible nitric oxide synthase), mitogen-activated protein kinase (MAPK)-p38 phosphorylation, and nuclear factor-κB (NF-κB) activation, was attenuated.
CONCLUSION—These findings suggested that long-term EECP exerts a retarding effect on atherosclerosis by downregulating proinflammatory gene expression. The underlying mechanisms are related to chronic exposure to increased pulsatile shear stress promoted by EECP; this exposure suppresses the overactivation of the MAPK-P38/NF-κB/VCAM-1 signaling pathway induced by hypercholesterolemia. |
| doi_str_mv | 10.1161/ATVBAHA.109.197806 |
| format | Article |
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METHODS AND RESULTS—Hypercholesterolemic pigs were subjected to a 7-week EECP intervention while being fed a high-cholesterol diet. EECP resulted in a 34.38% increase of mean wall shear stress and a significantly lower pulsatility index in the brachial artery. The animals receiving EECP showed a marked reduction in atherosclerotic lesion size in the coronary artery and abdominal aorta compared with the hypercholesterolemic control group, associated with a decrease in macrophage accumulation. The expression of a set of genes involved in inflammation (including C-reactive protein [CRP], complement 3a, vascular cell adhesion molecule-1 [VCAM-1], and inducible nitric oxide synthase), mitogen-activated protein kinase (MAPK)-p38 phosphorylation, and nuclear factor-κB (NF-κB) activation, was attenuated.
CONCLUSION—These findings suggested that long-term EECP exerts a retarding effect on atherosclerosis by downregulating proinflammatory gene expression. The underlying mechanisms are related to chronic exposure to increased pulsatile shear stress promoted by EECP; this exposure suppresses the overactivation of the MAPK-P38/NF-κB/VCAM-1 signaling pathway induced by hypercholesterolemia.</description><identifier>ISSN: 1079-5642</identifier><identifier>EISSN: 1524-4636</identifier><identifier>DOI: 10.1161/ATVBAHA.109.197806</identifier><identifier>PMID: 20150561</identifier><identifier>CODEN: ATVBFA</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Animals ; Aortic Diseases - immunology ; Aortic Diseases - metabolism ; Aortic Diseases - physiopathology ; Aortic Diseases - prevention & control ; Arteries - immunology ; Arteries - metabolism ; Arteries - pathology ; Arteries - physiopathology ; Atherosclerosis (general aspects, experimental research) ; Atherosclerosis - immunology ; Atherosclerosis - metabolism ; Atherosclerosis - physiopathology ; Atherosclerosis - prevention & control ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood Flow Velocity ; C-Reactive Protein - genetics ; Cardiology. Vascular system ; Cholesterol - blood ; Complement C3a - genetics ; Coronary Artery Disease - immunology ; Coronary Artery Disease - metabolism ; Coronary Artery Disease - physiopathology ; Coronary Artery Disease - prevention & control ; Counterpulsation ; Disease Models, Animal ; Disease Progression ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Gene Expression Regulation ; Hypercholesterolemia - complications ; Hypercholesterolemia - immunology ; Hypercholesterolemia - metabolism ; Hypercholesterolemia - physiopathology ; Hypercholesterolemia - therapy ; Inflammation Mediators - metabolism ; Male ; Medical sciences ; Neurology ; NF-kappa B - metabolism ; Nitric Oxide Synthase Type II - genetics ; p38 Mitogen-Activated Protein Kinases - metabolism ; Phosphorylation ; Pulsatile Flow ; Regional Blood Flow ; Signal Transduction - genetics ; Stress, Mechanical ; Sus scrofa ; Time Factors ; Vascular Cell Adhesion Molecule-1 - genetics ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Arteriosclerosis, thrombosis, and vascular biology, 2010-04, Vol.30 (4), p.773-780</ispartof><rights>2010 American Heart Association, Inc.</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4701-ee2d3e05f856b3992fd7dcbfe2c1cbde6a6c143ccf3599a3887f9fac7f9ea2553</citedby><cites>FETCH-LOGICAL-c4701-ee2d3e05f856b3992fd7dcbfe2c1cbde6a6c143ccf3599a3887f9fac7f9ea2553</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22545850$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20150561$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Yan</creatorcontrib><creatorcontrib>He, Xiaohong</creatorcontrib><creatorcontrib>Liu, Donghong</creatorcontrib><creatorcontrib>Wu, Guifu</creatorcontrib><creatorcontrib>Chen, Xiaolin</creatorcontrib><creatorcontrib>Ma, Hong</creatorcontrib><creatorcontrib>Du, Zhimin</creatorcontrib><creatorcontrib>Dong, Yugang</creatorcontrib><creatorcontrib>Jin, Yafei</creatorcontrib><creatorcontrib>He, Wen</creatorcontrib><creatorcontrib>Wang, Kuijian</creatorcontrib><creatorcontrib>Lawson, William E</creatorcontrib><creatorcontrib>Hui, John C.K</creatorcontrib><creatorcontrib>Zheng, Zhensheng</creatorcontrib><title>Enhanced External Counterpulsation Attenuates Atherosclerosis Progression Through Modulation of Proinflammatory Signal Pathway</title><title>Arteriosclerosis, thrombosis, and vascular biology</title><addtitle>Arterioscler Thromb Vasc Biol</addtitle><description>OBJECTIVE—Shear stress may be the most crucial local factor affecting atherogenesis. The present study investigated the effect of exposure to increased shear stress promoted by enhanced external counterpulsation (EECP) on the progression of atherosclerosis and the underlying inflammation-related molecular mechanisms in a porcine model of hypercholesterolemia.
METHODS AND RESULTS—Hypercholesterolemic pigs were subjected to a 7-week EECP intervention while being fed a high-cholesterol diet. EECP resulted in a 34.38% increase of mean wall shear stress and a significantly lower pulsatility index in the brachial artery. The animals receiving EECP showed a marked reduction in atherosclerotic lesion size in the coronary artery and abdominal aorta compared with the hypercholesterolemic control group, associated with a decrease in macrophage accumulation. The expression of a set of genes involved in inflammation (including C-reactive protein [CRP], complement 3a, vascular cell adhesion molecule-1 [VCAM-1], and inducible nitric oxide synthase), mitogen-activated protein kinase (MAPK)-p38 phosphorylation, and nuclear factor-κB (NF-κB) activation, was attenuated.
CONCLUSION—These findings suggested that long-term EECP exerts a retarding effect on atherosclerosis by downregulating proinflammatory gene expression. The underlying mechanisms are related to chronic exposure to increased pulsatile shear stress promoted by EECP; this exposure suppresses the overactivation of the MAPK-P38/NF-κB/VCAM-1 signaling pathway induced by hypercholesterolemia.</description><subject>Animals</subject><subject>Aortic Diseases - immunology</subject><subject>Aortic Diseases - metabolism</subject><subject>Aortic Diseases - physiopathology</subject><subject>Aortic Diseases - prevention & control</subject><subject>Arteries - immunology</subject><subject>Arteries - metabolism</subject><subject>Arteries - pathology</subject><subject>Arteries - physiopathology</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Atherosclerosis - immunology</subject><subject>Atherosclerosis - metabolism</subject><subject>Atherosclerosis - physiopathology</subject><subject>Atherosclerosis - prevention & control</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood Flow Velocity</subject><subject>C-Reactive Protein - genetics</subject><subject>Cardiology. Vascular system</subject><subject>Cholesterol - blood</subject><subject>Complement C3a - genetics</subject><subject>Coronary Artery Disease - immunology</subject><subject>Coronary Artery Disease - metabolism</subject><subject>Coronary Artery Disease - physiopathology</subject><subject>Coronary Artery Disease - prevention & control</subject><subject>Counterpulsation</subject><subject>Disease Models, Animal</subject><subject>Disease Progression</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Gene Expression Regulation</subject><subject>Hypercholesterolemia - complications</subject><subject>Hypercholesterolemia - immunology</subject><subject>Hypercholesterolemia - metabolism</subject><subject>Hypercholesterolemia - physiopathology</subject><subject>Hypercholesterolemia - therapy</subject><subject>Inflammation Mediators - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Neurology</subject><subject>NF-kappa B - metabolism</subject><subject>Nitric Oxide Synthase Type II - genetics</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Phosphorylation</subject><subject>Pulsatile Flow</subject><subject>Regional Blood Flow</subject><subject>Signal Transduction - genetics</subject><subject>Stress, Mechanical</subject><subject>Sus scrofa</subject><subject>Time Factors</subject><subject>Vascular Cell Adhesion Molecule-1 - genetics</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>1079-5642</issn><issn>1524-4636</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkUuP0zAUhS3EiHnxB1igbBCrFD9iJ1mGqjBIg2akKWwt17luAk5c7FilG377OEqBha_Plb57LJ-L0BuCV4QI8qHZfv_Y3DUrgusVqcsKixfoinBa5IVg4mXSuKxzLgp6ia5D-IExLijFr9AlxYRjLsgV-rMZOzVqaLPN7wn8qGy2dnFM8hBtUFPvxqyZJhijmiAk2YF3Qdu59iF79G7vIYQZ23bexX2XfXVttMukMzPRj8aqYVCT86fsqd_PjzyqqTuq0y26MMoGeH2-b9C3T5vt-i6_f_j8Zd3c57ooMckBaMsAc1NxsWN1TU1btnpngGqidy0IJTQpmNaG8bpWrKpKUxulUwVFOWc36P3ie_DuV4QwyaEPGqxVI7gYZMlYWdGUVCLpQur0w-DByIPvB-VPkmA5xy7Psae-lkvsaejt2T7uBmj_jfzNOQHvzoAKWlnjU-Z9-M9RXvCK48QVC3d0Nu0g_LTxCF52oOzUyXmBTGCeJ98kU5unQwl7Bh4znyQ</recordid><startdate>201004</startdate><enddate>201004</enddate><creator>Zhang, Yan</creator><creator>He, Xiaohong</creator><creator>Liu, Donghong</creator><creator>Wu, Guifu</creator><creator>Chen, Xiaolin</creator><creator>Ma, Hong</creator><creator>Du, Zhimin</creator><creator>Dong, Yugang</creator><creator>Jin, Yafei</creator><creator>He, Wen</creator><creator>Wang, Kuijian</creator><creator>Lawson, William E</creator><creator>Hui, John C.K</creator><creator>Zheng, Zhensheng</creator><general>American Heart Association, Inc</general><general>Lippincott Williams & Wilkins</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>201004</creationdate><title>Enhanced External Counterpulsation Attenuates Atherosclerosis Progression Through Modulation of Proinflammatory Signal Pathway</title><author>Zhang, Yan ; He, Xiaohong ; Liu, Donghong ; Wu, Guifu ; Chen, Xiaolin ; Ma, Hong ; Du, Zhimin ; Dong, Yugang ; Jin, Yafei ; He, Wen ; Wang, Kuijian ; Lawson, William E ; Hui, John C.K ; Zheng, Zhensheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4701-ee2d3e05f856b3992fd7dcbfe2c1cbde6a6c143ccf3599a3887f9fac7f9ea2553</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Animals</topic><topic>Aortic Diseases - immunology</topic><topic>Aortic Diseases - metabolism</topic><topic>Aortic Diseases - physiopathology</topic><topic>Aortic Diseases - prevention & control</topic><topic>Arteries - immunology</topic><topic>Arteries - metabolism</topic><topic>Arteries - pathology</topic><topic>Arteries - physiopathology</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Atherosclerosis - immunology</topic><topic>Atherosclerosis - metabolism</topic><topic>Atherosclerosis - physiopathology</topic><topic>Atherosclerosis - prevention & control</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood Flow Velocity</topic><topic>C-Reactive Protein - genetics</topic><topic>Cardiology. Vascular system</topic><topic>Cholesterol - blood</topic><topic>Complement C3a - genetics</topic><topic>Coronary Artery Disease - immunology</topic><topic>Coronary Artery Disease - metabolism</topic><topic>Coronary Artery Disease - physiopathology</topic><topic>Coronary Artery Disease - prevention & control</topic><topic>Counterpulsation</topic><topic>Disease Models, Animal</topic><topic>Disease Progression</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Gene Expression Regulation</topic><topic>Hypercholesterolemia - complications</topic><topic>Hypercholesterolemia - immunology</topic><topic>Hypercholesterolemia - metabolism</topic><topic>Hypercholesterolemia - physiopathology</topic><topic>Hypercholesterolemia - therapy</topic><topic>Inflammation Mediators - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Neurology</topic><topic>NF-kappa B - metabolism</topic><topic>Nitric Oxide Synthase Type II - genetics</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Phosphorylation</topic><topic>Pulsatile Flow</topic><topic>Regional Blood Flow</topic><topic>Signal Transduction - genetics</topic><topic>Stress, Mechanical</topic><topic>Sus scrofa</topic><topic>Time Factors</topic><topic>Vascular Cell Adhesion Molecule-1 - genetics</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Yan</creatorcontrib><creatorcontrib>He, Xiaohong</creatorcontrib><creatorcontrib>Liu, Donghong</creatorcontrib><creatorcontrib>Wu, Guifu</creatorcontrib><creatorcontrib>Chen, Xiaolin</creatorcontrib><creatorcontrib>Ma, Hong</creatorcontrib><creatorcontrib>Du, Zhimin</creatorcontrib><creatorcontrib>Dong, Yugang</creatorcontrib><creatorcontrib>Jin, Yafei</creatorcontrib><creatorcontrib>He, Wen</creatorcontrib><creatorcontrib>Wang, Kuijian</creatorcontrib><creatorcontrib>Lawson, William E</creatorcontrib><creatorcontrib>Hui, John C.K</creatorcontrib><creatorcontrib>Zheng, Zhensheng</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>Arteriosclerosis, thrombosis, and vascular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Yan</au><au>He, Xiaohong</au><au>Liu, Donghong</au><au>Wu, Guifu</au><au>Chen, Xiaolin</au><au>Ma, Hong</au><au>Du, Zhimin</au><au>Dong, Yugang</au><au>Jin, Yafei</au><au>He, Wen</au><au>Wang, Kuijian</au><au>Lawson, William E</au><au>Hui, John C.K</au><au>Zheng, Zhensheng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Enhanced External Counterpulsation Attenuates Atherosclerosis Progression Through Modulation of Proinflammatory Signal Pathway</atitle><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle><addtitle>Arterioscler Thromb Vasc Biol</addtitle><date>2010-04</date><risdate>2010</risdate><volume>30</volume><issue>4</issue><spage>773</spage><epage>780</epage><pages>773-780</pages><issn>1079-5642</issn><eissn>1524-4636</eissn><coden>ATVBFA</coden><abstract>OBJECTIVE—Shear stress may be the most crucial local factor affecting atherogenesis. The present study investigated the effect of exposure to increased shear stress promoted by enhanced external counterpulsation (EECP) on the progression of atherosclerosis and the underlying inflammation-related molecular mechanisms in a porcine model of hypercholesterolemia.
METHODS AND RESULTS—Hypercholesterolemic pigs were subjected to a 7-week EECP intervention while being fed a high-cholesterol diet. EECP resulted in a 34.38% increase of mean wall shear stress and a significantly lower pulsatility index in the brachial artery. The animals receiving EECP showed a marked reduction in atherosclerotic lesion size in the coronary artery and abdominal aorta compared with the hypercholesterolemic control group, associated with a decrease in macrophage accumulation. The expression of a set of genes involved in inflammation (including C-reactive protein [CRP], complement 3a, vascular cell adhesion molecule-1 [VCAM-1], and inducible nitric oxide synthase), mitogen-activated protein kinase (MAPK)-p38 phosphorylation, and nuclear factor-κB (NF-κB) activation, was attenuated.
CONCLUSION—These findings suggested that long-term EECP exerts a retarding effect on atherosclerosis by downregulating proinflammatory gene expression. The underlying mechanisms are related to chronic exposure to increased pulsatile shear stress promoted by EECP; this exposure suppresses the overactivation of the MAPK-P38/NF-κB/VCAM-1 signaling pathway induced by hypercholesterolemia.</abstract><cop>Philadelphia, PA</cop><pub>American Heart Association, Inc</pub><pmid>20150561</pmid><doi>10.1161/ATVBAHA.109.197806</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Arteriosclerosis, thrombosis, and vascular biology, 2010-04, Vol.30 (4), p.773-780 |
| issn | 1079-5642 1524-4636 |
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| subjects | Animals Aortic Diseases - immunology Aortic Diseases - metabolism Aortic Diseases - physiopathology Aortic Diseases - prevention & control Arteries - immunology Arteries - metabolism Arteries - pathology Arteries - physiopathology Atherosclerosis (general aspects, experimental research) Atherosclerosis - immunology Atherosclerosis - metabolism Atherosclerosis - physiopathology Atherosclerosis - prevention & control Biological and medical sciences Blood and lymphatic vessels Blood Flow Velocity C-Reactive Protein - genetics Cardiology. Vascular system Cholesterol - blood Complement C3a - genetics Coronary Artery Disease - immunology Coronary Artery Disease - metabolism Coronary Artery Disease - physiopathology Coronary Artery Disease - prevention & control Counterpulsation Disease Models, Animal Disease Progression Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Gene Expression Regulation Hypercholesterolemia - complications Hypercholesterolemia - immunology Hypercholesterolemia - metabolism Hypercholesterolemia - physiopathology Hypercholesterolemia - therapy Inflammation Mediators - metabolism Male Medical sciences Neurology NF-kappa B - metabolism Nitric Oxide Synthase Type II - genetics p38 Mitogen-Activated Protein Kinases - metabolism Phosphorylation Pulsatile Flow Regional Blood Flow Signal Transduction - genetics Stress, Mechanical Sus scrofa Time Factors Vascular Cell Adhesion Molecule-1 - genetics Vascular diseases and vascular malformations of the nervous system |
| title | Enhanced External Counterpulsation Attenuates Atherosclerosis Progression Through Modulation of Proinflammatory Signal Pathway |
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