Pioglitazone Improves Aortic Wall Elasticity in a Rat Model of Elastocalcinotic Arteriosclerosis
Specific treatment of age-related aortic wall arteriosclerosis and stiffening is lacking. Because ligands for peroxisome proliferator–activated receptor γ have beneficial effects on the arterial wall in atherosclerosis, via an antiinflammatory mechanism, we investigated whether long-term pioglitazon...
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| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2005-08, Vol.46 (2), p.372-379 |
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| container_title | Hypertension (Dallas, Tex. 1979) |
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| creator | Gaillard, Virginie Casellas, Daniel Seguin-Devaux, Carole Schohn, Hervé Dauça, Michel Atkinson, Jeffrey Lartaud, Isabelle |
| description | Specific treatment of age-related aortic wall arteriosclerosis and stiffening is lacking. Because ligands for peroxisome proliferator–activated receptor γ have beneficial effects on the arterial wall in atherosclerosis, via an antiinflammatory mechanism, we investigated whether long-term pioglitazone (Pio) treatment protects against another form of vascular wall disease, arteriosclerosis. We evaluated, in a rat model of elastocalcinotic arteriosclerosis (hypervitaminosis D and nicotine [VDN]), whether Pio (3 mg · kg per day for 1.5 month PO) attenuated arteriosclerosis and its consequencesaortic wall rigidity, increased aortic pulse pressure, and left ventricular hypertrophy. In VDN rats, medial calcification was associated with monocyte/macrophage infiltration and induction of tumor necrosis factor α and interleukin 1β. Pio increased nuclear peroxisome proliferator–activated receptor γ immunostaining in the aortic wall, decreased tumor necrosis factor α (P |
| doi_str_mv | 10.1161/01.HYP.0000171472.24422.33 |
| format | Article |
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Because ligands for peroxisome proliferator–activated receptor γ have beneficial effects on the arterial wall in atherosclerosis, via an antiinflammatory mechanism, we investigated whether long-term pioglitazone (Pio) treatment protects against another form of vascular wall disease, arteriosclerosis. We evaluated, in a rat model of elastocalcinotic arteriosclerosis (hypervitaminosis D and nicotine [VDN]), whether Pio (3 mg · kg per day for 1.5 month PO) attenuated arteriosclerosis and its consequencesaortic wall rigidity, increased aortic pulse pressure, and left ventricular hypertrophy. In VDN rats, medial calcification was associated with monocyte/macrophage infiltration and induction of tumor necrosis factor α and interleukin 1β. Pio increased nuclear peroxisome proliferator–activated receptor γ immunostaining in the aortic wall, decreased tumor necrosis factor α (P<0.05 versus VDN Pio), tended to decrease interleukin 1β mRNA expression (P=0.08 versus VDN Pio), blunted aortic wall calcification (271±69, P<0.05 versus VDN Pio 562±87 μmol · g dry weight) and prevented fragmentation of elastic fibers (segments per 10 000 μm8.4±0.3; P<0.05 versus VDN Pio 10.5±0.6). Pio reduced aortic wall stiffness (elastic modulus/wall stress4.8±0.6; P<0.05 versus VDN Pio 10.0±1.6), aortic pulse pressure (30±2 mm Hg; P<0.05 versus VDN Pio 39±4) and left ventricular hypertrophy (1.58±0.05 g · kg; P<0.05 versus VDN Pio 1.76±0.06). In conclusion, long-term Pio treatment attenuates aortic wall elastocalcinosis and, thus, lowers aortic wall stiffness, aortic pulse pressure, and left ventricular hypertrophy.]]></description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/01.HYP.0000171472.24422.33</identifier><identifier>PMID: 15967870</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Animals ; Aorta - pathology ; Aorta - physiopathology ; Aorta, Thoracic - metabolism ; Aorta, Thoracic - pathology ; Aortic Diseases - pathology ; Aortic Diseases - physiopathology ; Arterial hypertension. Arterial hypotension ; Arteriosclerosis - pathology ; Arteriosclerosis - physiopathology ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood Pressure - drug effects ; Calcinosis - pathology ; Calcinosis - physiopathology ; Cardiology. Vascular system ; Clinical manifestations. Epidemiology. Investigative techniques. Etiology ; Cytokines - metabolism ; Elastic Tissue - pathology ; Elastic Tissue - physiopathology ; Elasticity ; Experimental diseases ; Hypertrophy, Left Ventricular - pathology ; Macrophages - pathology ; Male ; Medical sciences ; Monocytes - pathology ; Myocardium - pathology ; Organ Size - drug effects ; PPAR gamma - metabolism ; Rats ; Rats, Wistar ; Thiazolidinediones - pharmacology</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2005-08, Vol.46 (2), p.372-379</ispartof><rights>2005 American Heart Association, Inc.</rights><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5516-612f52d0f6a92a1fc48a5f975216969033537109ba67aa5a3a0e3171785f85cf3</citedby><cites>FETCH-LOGICAL-c5516-612f52d0f6a92a1fc48a5f975216969033537109ba67aa5a3a0e3171785f85cf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3687,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17016637$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15967870$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gaillard, Virginie</creatorcontrib><creatorcontrib>Casellas, Daniel</creatorcontrib><creatorcontrib>Seguin-Devaux, Carole</creatorcontrib><creatorcontrib>Schohn, Hervé</creatorcontrib><creatorcontrib>Dauça, Michel</creatorcontrib><creatorcontrib>Atkinson, Jeffrey</creatorcontrib><creatorcontrib>Lartaud, Isabelle</creatorcontrib><title>Pioglitazone Improves Aortic Wall Elasticity in a Rat Model of Elastocalcinotic Arteriosclerosis</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description><![CDATA[Specific treatment of age-related aortic wall arteriosclerosis and stiffening is lacking. Because ligands for peroxisome proliferator–activated receptor γ have beneficial effects on the arterial wall in atherosclerosis, via an antiinflammatory mechanism, we investigated whether long-term pioglitazone (Pio) treatment protects against another form of vascular wall disease, arteriosclerosis. We evaluated, in a rat model of elastocalcinotic arteriosclerosis (hypervitaminosis D and nicotine [VDN]), whether Pio (3 mg · kg per day for 1.5 month PO) attenuated arteriosclerosis and its consequencesaortic wall rigidity, increased aortic pulse pressure, and left ventricular hypertrophy. In VDN rats, medial calcification was associated with monocyte/macrophage infiltration and induction of tumor necrosis factor α and interleukin 1β. Pio increased nuclear peroxisome proliferator–activated receptor γ immunostaining in the aortic wall, decreased tumor necrosis factor α (P<0.05 versus VDN Pio), tended to decrease interleukin 1β mRNA expression (P=0.08 versus VDN Pio), blunted aortic wall calcification (271±69, P<0.05 versus VDN Pio 562±87 μmol · g dry weight) and prevented fragmentation of elastic fibers (segments per 10 000 μm8.4±0.3; P<0.05 versus VDN Pio 10.5±0.6). Pio reduced aortic wall stiffness (elastic modulus/wall stress4.8±0.6; P<0.05 versus VDN Pio 10.0±1.6), aortic pulse pressure (30±2 mm Hg; P<0.05 versus VDN Pio 39±4) and left ventricular hypertrophy (1.58±0.05 g · kg; P<0.05 versus VDN Pio 1.76±0.06). In conclusion, long-term Pio treatment attenuates aortic wall elastocalcinosis and, thus, lowers aortic wall stiffness, aortic pulse pressure, and left ventricular hypertrophy.]]></description><subject>Animals</subject><subject>Aorta - pathology</subject><subject>Aorta - physiopathology</subject><subject>Aorta, Thoracic - metabolism</subject><subject>Aorta, Thoracic - pathology</subject><subject>Aortic Diseases - pathology</subject><subject>Aortic Diseases - physiopathology</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Arteriosclerosis - pathology</subject><subject>Arteriosclerosis - physiopathology</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood Pressure - drug effects</subject><subject>Calcinosis - pathology</subject><subject>Calcinosis - physiopathology</subject><subject>Cardiology. Vascular system</subject><subject>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</subject><subject>Cytokines - metabolism</subject><subject>Elastic Tissue - pathology</subject><subject>Elastic Tissue - physiopathology</subject><subject>Elasticity</subject><subject>Experimental diseases</subject><subject>Hypertrophy, Left Ventricular - pathology</subject><subject>Macrophages - pathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Monocytes - pathology</subject><subject>Myocardium - pathology</subject><subject>Organ Size - drug effects</subject><subject>PPAR gamma - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Thiazolidinediones - pharmacology</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkFtrFDEUgIModlv9CzII-jZjTq4T35ZSbaFiEUV9iqfZxEazkzaZtbS_3rS7sIEQDvnO7SPkNdABQME7CsPpz4uBtgMahGYDE4KxgfMnZAGSiV5IxZ-SBQUjegPw44Ac1vqn4UII_ZwcgDRKj5ouyK-LmH-nOON9nnx3tr4u-Z-v3TKXObruO6bUnSSsLYjzXRenDrsvOHef8sqnLoftZ3aYXJzyQ8qyzL7EXF3yJddYX5BnAVP1L3fvEfn24eTr8Wl__vnj2fHyvHdSguoVsCDZigaFhiEEJ0aUwWjJQBllKOeSa6DmEpVGlMiRet6216MMo3SBH5G327ptg5uNr7Ndx-p8Sjj5vKlWjXQ0jKkGvt-Crs1Xiw_2usQ1ljsL1D74tRRs82v3fu2jX8t5S36167K5XPvVPnUntAFvdgDWZiUUnFyse05TUIrrxoktd5tTE1b_ps2tL_bKY5qvHlsLpsaeUSrp2KK-3Tb8f_hBkxQ</recordid><startdate>200508</startdate><enddate>200508</enddate><creator>Gaillard, Virginie</creator><creator>Casellas, Daniel</creator><creator>Seguin-Devaux, Carole</creator><creator>Schohn, Hervé</creator><creator>Dauça, Michel</creator><creator>Atkinson, Jeffrey</creator><creator>Lartaud, Isabelle</creator><general>American Heart Association, Inc</general><general>Lippincott</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>200508</creationdate><title>Pioglitazone Improves Aortic Wall Elasticity in a Rat Model of Elastocalcinotic Arteriosclerosis</title><author>Gaillard, Virginie ; Casellas, Daniel ; Seguin-Devaux, Carole ; Schohn, Hervé ; Dauça, Michel ; Atkinson, Jeffrey ; Lartaud, Isabelle</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5516-612f52d0f6a92a1fc48a5f975216969033537109ba67aa5a3a0e3171785f85cf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Aorta - pathology</topic><topic>Aorta - physiopathology</topic><topic>Aorta, Thoracic - metabolism</topic><topic>Aorta, Thoracic - pathology</topic><topic>Aortic Diseases - pathology</topic><topic>Aortic Diseases - physiopathology</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Arteriosclerosis - pathology</topic><topic>Arteriosclerosis - physiopathology</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood Pressure - drug effects</topic><topic>Calcinosis - pathology</topic><topic>Calcinosis - physiopathology</topic><topic>Cardiology. Vascular system</topic><topic>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</topic><topic>Cytokines - metabolism</topic><topic>Elastic Tissue - pathology</topic><topic>Elastic Tissue - physiopathology</topic><topic>Elasticity</topic><topic>Experimental diseases</topic><topic>Hypertrophy, Left Ventricular - pathology</topic><topic>Macrophages - pathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Monocytes - pathology</topic><topic>Myocardium - pathology</topic><topic>Organ Size - drug effects</topic><topic>PPAR gamma - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Thiazolidinediones - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gaillard, Virginie</creatorcontrib><creatorcontrib>Casellas, Daniel</creatorcontrib><creatorcontrib>Seguin-Devaux, Carole</creatorcontrib><creatorcontrib>Schohn, Hervé</creatorcontrib><creatorcontrib>Dauça, Michel</creatorcontrib><creatorcontrib>Atkinson, Jeffrey</creatorcontrib><creatorcontrib>Lartaud, Isabelle</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>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gaillard, Virginie</au><au>Casellas, Daniel</au><au>Seguin-Devaux, Carole</au><au>Schohn, Hervé</au><au>Dauça, Michel</au><au>Atkinson, Jeffrey</au><au>Lartaud, Isabelle</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pioglitazone Improves Aortic Wall Elasticity in a Rat Model of Elastocalcinotic Arteriosclerosis</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>2005-08</date><risdate>2005</risdate><volume>46</volume><issue>2</issue><spage>372</spage><epage>379</epage><pages>372-379</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract><![CDATA[Specific treatment of age-related aortic wall arteriosclerosis and stiffening is lacking. Because ligands for peroxisome proliferator–activated receptor γ have beneficial effects on the arterial wall in atherosclerosis, via an antiinflammatory mechanism, we investigated whether long-term pioglitazone (Pio) treatment protects against another form of vascular wall disease, arteriosclerosis. We evaluated, in a rat model of elastocalcinotic arteriosclerosis (hypervitaminosis D and nicotine [VDN]), whether Pio (3 mg · kg per day for 1.5 month PO) attenuated arteriosclerosis and its consequencesaortic wall rigidity, increased aortic pulse pressure, and left ventricular hypertrophy. In VDN rats, medial calcification was associated with monocyte/macrophage infiltration and induction of tumor necrosis factor α and interleukin 1β. Pio increased nuclear peroxisome proliferator–activated receptor γ immunostaining in the aortic wall, decreased tumor necrosis factor α (P<0.05 versus VDN Pio), tended to decrease interleukin 1β mRNA expression (P=0.08 versus VDN Pio), blunted aortic wall calcification (271±69, P<0.05 versus VDN Pio 562±87 μmol · g dry weight) and prevented fragmentation of elastic fibers (segments per 10 000 μm8.4±0.3; P<0.05 versus VDN Pio 10.5±0.6). Pio reduced aortic wall stiffness (elastic modulus/wall stress4.8±0.6; P<0.05 versus VDN Pio 10.0±1.6), aortic pulse pressure (30±2 mm Hg; P<0.05 versus VDN Pio 39±4) and left ventricular hypertrophy (1.58±0.05 g · kg; P<0.05 versus VDN Pio 1.76±0.06). In conclusion, long-term Pio treatment attenuates aortic wall elastocalcinosis and, thus, lowers aortic wall stiffness, aortic pulse pressure, and left ventricular hypertrophy.]]></abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>15967870</pmid><doi>10.1161/01.HYP.0000171472.24422.33</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Aorta - pathology Aorta - physiopathology Aorta, Thoracic - metabolism Aorta, Thoracic - pathology Aortic Diseases - pathology Aortic Diseases - physiopathology Arterial hypertension. Arterial hypotension Arteriosclerosis - pathology Arteriosclerosis - physiopathology Biological and medical sciences Blood and lymphatic vessels Blood Pressure - drug effects Calcinosis - pathology Calcinosis - physiopathology Cardiology. Vascular system Clinical manifestations. Epidemiology. Investigative techniques. Etiology Cytokines - metabolism Elastic Tissue - pathology Elastic Tissue - physiopathology Elasticity Experimental diseases Hypertrophy, Left Ventricular - pathology Macrophages - pathology Male Medical sciences Monocytes - pathology Myocardium - pathology Organ Size - drug effects PPAR gamma - metabolism Rats Rats, Wistar Thiazolidinediones - pharmacology |
| title | Pioglitazone Improves Aortic Wall Elasticity in a Rat Model of Elastocalcinotic Arteriosclerosis |
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