AustralieFrV1, PascalFrancis, Corpus, bibRecord, 002828

Angiotensin II subtype 2 receptor blockade and deficiency attenuate the development of atherosclerosis in an apolipoprotein E-deficient mouse model of diabetes

Identifieur interne : 002828 ( PascalFrancis/Corpus ); précédent : 002827; suivant : 002829

Angiotensin II subtype 2 receptor blockade and deficiency attenuate the development of atherosclerosis in an apolipoprotein E-deficient mouse model of diabetes

Auteurs : A. Koïtka ; Z. Cao ; P. Koh ; A. M. D. Watson ; K. C. Sourris ; L. Loufrani ; A. Soro-Paavonen ; T. Walther ; K. J. Woollard ; K. A. M. Jandeleit-Dahm ; M. E. Cooper ; T. J. Allen

Source :

Diabetologia : (Berlin) [ 0012-186X ] ; 2010.

RBID : Pascal:10-0128283

Descripteurs français

Pascal (Inist)
- Angiotensine II, Soustype, Récepteur biologique, Déficit, Développement, Apolipoprotéine E, Athérosclérose, Animal, Diabète, Modèle animal, Souris.

English descriptors

KwdEn :
- Angiotensin II, Animal, Animal model, Apolipoprotein E, Atherosclerosis, Biological receptor, Deficiency, Development, Diabetes mellitus, Mouse, Subtype.

Abstract

Aims/hypothesis Most of the known actions of angiotensin II have been considered primarily to be the result of angiotensin II subtype 1 receptor activation. However, recent data suggest that the angiotensin II subtype 2 receptor (AT₂R) may modulate key processes linked to atherosclerosis. The aim of this study was to investigate the role of AT₂R in diabetes-associated atherosclerosis using pharmacological blockade and genetic deficiency. Methods Aortic plaque deposition was assessed in streptozotocin-induced diabetic apolipoprotein E (Apoe) knockout (KO) and At₂r (also known as Agtr2)/Apoe double-KO (DKO) mice. Control and diabetic Apoe-KO mice received an AT₂R antagonist PD123319 (5 mg kg^-1 day^-1) via osmotic minipump for 20 weeks (n=7-8 per group). Results Diabetes was associated with a sixfold increase in plaque area (diabetic Apoe-KO: 12.7±1.4% vs control Apoe-KO: 2.3±0.4%, p<0.001) as well as a significant increase in aortic expression of the gene At₂r (also known as Agtr2). The increase in plaque area with diabetes was attenuated in AT₂R antagonist-treated diabetic Apoe-KO mice (7.1±0.5%, p<0.05) and in diabetic At₂r/Apoe DKO mice (9.2±1.3%, p<0.05). These benefits occurred independently of glycaemic control or BP, and were associated with downregulation of a range of pro-inflammatory cytokines, adhesion molecules, chemokines and various extracellular matrix proteins. Conclusionslinterpretation This study provides evidence for AT₂R playing a role in the development of diabetes-associated atherosclerosis. These findings suggest a potential utility of AT₂R blockers in the prevention and treatment of diabetic macrovascular complications.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A14	`02`			`@1 Department of Integrated Neurovascular Biology, University of Angers @2 Angers @3 FRA @Z 6 aut.`
A14	`03`			`@1 Department of Biomedical Sciences, Hull York Medical School, University of Hull @2 Hull @3 GBR @Z 8 aut.`
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C01	`01`		`ENG`	@0 Aims/hypothesis Most of the known actions of angiotensin II have been considered primarily to be the result of angiotensin II subtype 1 receptor activation. However, recent data suggest that the angiotensin II subtype 2 receptor (AT₂R) may modulate key processes linked to atherosclerosis. The aim of this study was to investigate the role of AT₂R in diabetes-associated atherosclerosis using pharmacological blockade and genetic deficiency. Methods Aortic plaque deposition was assessed in streptozotocin-induced diabetic apolipoprotein E (Apoe) knockout (KO) and At₂r (also known as Agtr2)/Apoe double-KO (DKO) mice. Control and diabetic Apoe-KO mice received an AT₂R antagonist PD123319 (5 mg kg^-1 day^-1) via osmotic minipump for 20 weeks (n=7-8 per group). Results Diabetes was associated with a sixfold increase in plaque area (diabetic Apoe-KO: 12.7±1.4% vs control Apoe-KO: 2.3±0.4%, p<0.001) as well as a significant increase in aortic expression of the gene At₂r (also known as Agtr2). The increase in plaque area with diabetes was attenuated in AT₂R antagonist-treated diabetic Apoe-KO mice (7.1±0.5%, p<0.05) and in diabetic At₂r/Apoe DKO mice (9.2±1.3%, p<0.05). These benefits occurred independently of glycaemic control or BP, and were associated with downregulation of a range of pro-inflammatory cytokines, adhesion molecules, chemokines and various extracellular matrix proteins. Conclusionslinterpretation This study provides evidence for AT₂R playing a role in the development of diabetes-associated atherosclerosis. These findings suggest a potential utility of AT₂R blockers in the prevention and treatment of diabetic macrovascular complications.
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Format Inist (serveur)

NO :	PASCAL 10-0128283 INIST
ET :	Angiotensin II subtype 2 receptor blockade and deficiency attenuate the development of atherosclerosis in an apolipoprotein E-deficient mouse model of diabetes
AU :	KOÏTKA (A.); CAO (Z.); KOH (P.); WATSON (A. M. D.); SOURRIS (K. C.); LOUFRANI (L.); SORO-PAAVONEN (A.); WALTHER (T.); WOOLLARD (K. J.); JANDELEIT-DAHM (K. A. M.); COOPER (M. E.); ALLEN (T. J.)
AF :	JDRF Danielle Alberti Memorial Centre for Diabetic Complications, Diabetes Division, Baker IDI Heart and Diabetes Research Institute, PO Box 6492, St Kilda Road Central/Melbourne, VIC 8008/Australie (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 7 aut., 10 aut., 11 aut., 12 aut.); Department of Integrated Neurovascular Biology, University of Angers/Angers/France (6 aut.); Department of Biomedical Sciences, Hull York Medical School, University of Hull/Hull/Royaume-Uni (8 aut.); Vascular Pharmacology, Baker IDI Heart and Diabetes Institute/Melbourne, VIC/Australie (9 aut.)
DT :	Publication en série; Niveau analytique
SO :	Diabetologia : (Berlin); ISSN 0012-186X; Allemagne; Da. 2010; Vol. 53; No. 3; Pp. 584-592; Bibl. 47 ref.
LA :	Anglais
EA :	Aims/hypothesis Most of the known actions of angiotensin II have been considered primarily to be the result of angiotensin II subtype 1 receptor activation. However, recent data suggest that the angiotensin II subtype 2 receptor (AT₂R) may modulate key processes linked to atherosclerosis. The aim of this study was to investigate the role of AT₂R in diabetes-associated atherosclerosis using pharmacological blockade and genetic deficiency. Methods Aortic plaque deposition was assessed in streptozotocin-induced diabetic apolipoprotein E (Apoe) knockout (KO) and At₂r (also known as Agtr2)/Apoe double-KO (DKO) mice. Control and diabetic Apoe-KO mice received an AT₂R antagonist PD123319 (5 mg kg^-1 day^-1) via osmotic minipump for 20 weeks (n=7-8 per group). Results Diabetes was associated with a sixfold increase in plaque area (diabetic Apoe-KO: 12.7±1.4% vs control Apoe-KO: 2.3±0.4%, p<0.001) as well as a significant increase in aortic expression of the gene At₂r (also known as Agtr2). The increase in plaque area with diabetes was attenuated in AT₂R antagonist-treated diabetic Apoe-KO mice (7.1±0.5%, p<0.05) and in diabetic At₂r/Apoe DKO mice (9.2±1.3%, p<0.05). These benefits occurred independently of glycaemic control or BP, and were associated with downregulation of a range of pro-inflammatory cytokines, adhesion molecules, chemokines and various extracellular matrix proteins. Conclusionslinterpretation This study provides evidence for AT₂R playing a role in the development of diabetes-associated atherosclerosis. These findings suggest a potential utility of AT₂R blockers in the prevention and treatment of diabetic macrovascular complications.
CC :	002B21E01A; 002B12B01
FD :	Angiotensine II; Soustype; Récepteur biologique; Déficit; Développement; Apolipoprotéine E; Athérosclérose; Animal; Diabète; Modèle animal; Souris
FG :	Hormone peptide; Octapeptide; Système renin angiotensine; Pathologie de l'appareil circulatoire; Pathologie des vaisseaux sanguins; Endocrinopathie; Rodentia; Mammalia; Vertebrata
ED :	Angiotensin II; Subtype; Biological receptor; Deficiency; Development; Apolipoprotein E; Atherosclerosis; Animal; Diabetes mellitus; Animal model; Mouse
EG :	Peptide hormone; Octapeptide; Renin angiotensin system; Cardiovascular disease; Vascular disease; Endocrinopathy; Rodentia; Mammalia; Vertebrata
SD :	Angiotensina II; Subtipo; Receptor biológico; Déficiencia; Desarrollo; Apolipoproteína E; Ateroesclerosis; Animal; Diabetes; Modelo animal; Ratón
LO :	INIST-13012.354000190030950240
ID :	10-0128283

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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Angiotensin II subtype 2 receptor blockade and deficiency attenuate the development of atherosclerosis in an apolipoprotein E-deficient mouse model of diabetes</title>
<author><name sortKey="Koitka, A" sort="Koitka, A" uniqKey="Koitka A" first="A." last="Koïtka">A. Koïtka</name>
<affiliation><inist:fA14 i1="01"><s1>JDRF Danielle Alberti Memorial Centre for Diabetic Complications, Diabetes Division, Baker IDI Heart and Diabetes Research Institute, PO Box 6492, St Kilda Road Central</s1>
<s2>Melbourne, VIC 8008</s2>
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<affiliation><inist:fA14 i1="01"><s1>JDRF Danielle Alberti Memorial Centre for Diabetic Complications, Diabetes Division, Baker IDI Heart and Diabetes Research Institute, PO Box 6492, St Kilda Road Central</s1>
<s2>Melbourne, VIC 8008</s2>
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<author><name sortKey="Koh, P" sort="Koh, P" uniqKey="Koh P" first="P." last="Koh">P. Koh</name>
<affiliation><inist:fA14 i1="01"><s1>JDRF Danielle Alberti Memorial Centre for Diabetic Complications, Diabetes Division, Baker IDI Heart and Diabetes Research Institute, PO Box 6492, St Kilda Road Central</s1>
<s2>Melbourne, VIC 8008</s2>
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<author><name sortKey="Watson, A M D" sort="Watson, A M D" uniqKey="Watson A" first="A. M. D." last="Watson">A. M. D. Watson</name>
<affiliation><inist:fA14 i1="01"><s1>JDRF Danielle Alberti Memorial Centre for Diabetic Complications, Diabetes Division, Baker IDI Heart and Diabetes Research Institute, PO Box 6492, St Kilda Road Central</s1>
<s2>Melbourne, VIC 8008</s2>
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<author><name sortKey="Sourris, K C" sort="Sourris, K C" uniqKey="Sourris K" first="K. C." last="Sourris">K. C. Sourris</name>
<affiliation><inist:fA14 i1="01"><s1>JDRF Danielle Alberti Memorial Centre for Diabetic Complications, Diabetes Division, Baker IDI Heart and Diabetes Research Institute, PO Box 6492, St Kilda Road Central</s1>
<s2>Melbourne, VIC 8008</s2>
<s3>AUS</s3>
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<author><name sortKey="Loufrani, L" sort="Loufrani, L" uniqKey="Loufrani L" first="L." last="Loufrani">L. Loufrani</name>
<affiliation><inist:fA14 i1="02"><s1>Department of Integrated Neurovascular Biology, University of Angers</s1>
<s2>Angers</s2>
<s3>FRA</s3>
<sZ>6 aut.</sZ>
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<author><name sortKey="Soro Paavonen, A" sort="Soro Paavonen, A" uniqKey="Soro Paavonen A" first="A." last="Soro-Paavonen">A. Soro-Paavonen</name>
<affiliation><inist:fA14 i1="01"><s1>JDRF Danielle Alberti Memorial Centre for Diabetic Complications, Diabetes Division, Baker IDI Heart and Diabetes Research Institute, PO Box 6492, St Kilda Road Central</s1>
<s2>Melbourne, VIC 8008</s2>
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<author><name sortKey="Walther, T" sort="Walther, T" uniqKey="Walther T" first="T." last="Walther">T. Walther</name>
<affiliation><inist:fA14 i1="03"><s1>Department of Biomedical Sciences, Hull York Medical School, University of Hull</s1>
<s2>Hull</s2>
<s3>GBR</s3>
<sZ>8 aut.</sZ>
</inist:fA14>
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<author><name sortKey="Woollard, K J" sort="Woollard, K J" uniqKey="Woollard K" first="K. J." last="Woollard">K. J. Woollard</name>
<affiliation><inist:fA14 i1="04"><s1>Vascular Pharmacology, Baker IDI Heart and Diabetes Institute</s1>
<s2>Melbourne, VIC</s2>
<s3>AUS</s3>
<sZ>9 aut.</sZ>
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<author><name sortKey="Jandeleit Dahm, K A M" sort="Jandeleit Dahm, K A M" uniqKey="Jandeleit Dahm K" first="K. A. M." last="Jandeleit-Dahm">K. A. M. Jandeleit-Dahm</name>
<affiliation><inist:fA14 i1="01"><s1>JDRF Danielle Alberti Memorial Centre for Diabetic Complications, Diabetes Division, Baker IDI Heart and Diabetes Research Institute, PO Box 6492, St Kilda Road Central</s1>
<s2>Melbourne, VIC 8008</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
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<sZ>5 aut.</sZ>
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<sZ>10 aut.</sZ>
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<author><name sortKey="Cooper, M E" sort="Cooper, M E" uniqKey="Cooper M" first="M. E." last="Cooper">M. E. Cooper</name>
<affiliation><inist:fA14 i1="01"><s1>JDRF Danielle Alberti Memorial Centre for Diabetic Complications, Diabetes Division, Baker IDI Heart and Diabetes Research Institute, PO Box 6492, St Kilda Road Central</s1>
<s2>Melbourne, VIC 8008</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
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<author><name sortKey="Allen, T J" sort="Allen, T J" uniqKey="Allen T" first="T. J." last="Allen">T. J. Allen</name>
<affiliation><inist:fA14 i1="01"><s1>JDRF Danielle Alberti Memorial Centre for Diabetic Complications, Diabetes Division, Baker IDI Heart and Diabetes Research Institute, PO Box 6492, St Kilda Road Central</s1>
<s2>Melbourne, VIC 8008</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>10 aut.</sZ>
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<series><title level="j" type="main">Diabetologia : (Berlin)</title>
<title level="j" type="abbreviated">Diabetologia : (Berl.)</title>
<idno type="ISSN">0012-186X</idno>
<imprint><date when="2010">2010</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><title level="j" type="main">Diabetologia : (Berlin)</title>
<title level="j" type="abbreviated">Diabetologia : (Berl.)</title>
<idno type="ISSN">0012-186X</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Angiotensin II</term>
<term>Animal</term>
<term>Animal model</term>
<term>Apolipoprotein E</term>
<term>Atherosclerosis</term>
<term>Biological receptor</term>
<term>Deficiency</term>
<term>Development</term>
<term>Diabetes mellitus</term>
<term>Mouse</term>
<term>Subtype</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Angiotensine II</term>
<term>Soustype</term>
<term>Récepteur biologique</term>
<term>Déficit</term>
<term>Développement</term>
<term>Apolipoprotéine E</term>
<term>Athérosclérose</term>
<term>Animal</term>
<term>Diabète</term>
<term>Modèle animal</term>
<term>Souris</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Aims/hypothesis Most of the known actions of angiotensin II have been considered primarily to be the result of angiotensin II subtype 1 receptor activation. However, recent data suggest that the angiotensin II subtype 2 receptor (AT<sub>2</sub>
R) may modulate key processes linked to atherosclerosis. The aim of this study was to investigate the role of AT<sub>2</sub>
R in diabetes-associated atherosclerosis using pharmacological blockade and genetic deficiency. Methods Aortic plaque deposition was assessed in streptozotocin-induced diabetic apolipoprotein E (Apoe) knockout (KO) and At<sub>2</sub>
r (also known as Agtr2)/Apoe double-KO (DKO) mice. Control and diabetic Apoe-KO mice received an AT<sub>2</sub>
R antagonist PD123319 (5 mg kg<sup>-1</sup>
 day<sup>-1</sup>
) via osmotic minipump for 20 weeks (n=7-8 per group). Results Diabetes was associated with a sixfold increase in plaque area (diabetic Apoe-KO: 12.7±1.4% vs control Apoe-KO: 2.3±0.4%, p<0.001) as well as a significant increase in aortic expression of the gene At<sub>2</sub>
r (also known as Agtr2). The increase in plaque area with diabetes was attenuated in AT<sub>2</sub>
R antagonist-treated diabetic Apoe-KO mice (7.1±0.5%, p<0.05) and in diabetic At<sub>2</sub>
r/Apoe DKO mice (9.2±1.3%, p<0.05). These benefits occurred independently of glycaemic control or BP, and were associated with downregulation of a range of pro-inflammatory cytokines, adhesion molecules, chemokines and various extracellular matrix proteins. Conclusionslinterpretation This study provides evidence for AT<sub>2</sub>
R playing a role in the development of diabetes-associated atherosclerosis. These findings suggest a potential utility of AT<sub>2</sub>
R blockers in the prevention and treatment of diabetic macrovascular complications.</div>
</front>
</TEI>
<inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0012-186X</s0>
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<fA03 i2="1"><s0>Diabetologia : (Berl.)</s0>
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<fA05><s2>53</s2>
</fA05>
<fA06><s2>3</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>Angiotensin II subtype 2 receptor blockade and deficiency attenuate the development of atherosclerosis in an apolipoprotein E-deficient mouse model of diabetes</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>KOÏTKA (A.)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>CAO (Z.)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>KOH (P.)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>WATSON (A. M. D.)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>SOURRIS (K. C.)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>LOUFRANI (L.)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>SORO-PAAVONEN (A.)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>WALTHER (T.)</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>WOOLLARD (K. J.)</s1>
</fA11>
<fA11 i1="10" i2="1"><s1>JANDELEIT-DAHM (K. A. M.)</s1>
</fA11>
<fA11 i1="11" i2="1"><s1>COOPER (M. E.)</s1>
</fA11>
<fA11 i1="12" i2="1"><s1>ALLEN (T. J.)</s1>
</fA11>
<fA14 i1="01"><s1>JDRF Danielle Alberti Memorial Centre for Diabetic Complications, Diabetes Division, Baker IDI Heart and Diabetes Research Institute, PO Box 6492, St Kilda Road Central</s1>
<s2>Melbourne, VIC 8008</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Department of Integrated Neurovascular Biology, University of Angers</s1>
<s2>Angers</s2>
<s3>FRA</s3>
<sZ>6 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Department of Biomedical Sciences, Hull York Medical School, University of Hull</s1>
<s2>Hull</s2>
<s3>GBR</s3>
<sZ>8 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Vascular Pharmacology, Baker IDI Heart and Diabetes Institute</s1>
<s2>Melbourne, VIC</s2>
<s3>AUS</s3>
<sZ>9 aut.</sZ>
</fA14>
<fA20><s1>584-592</s1>
</fA20>
<fA21><s1>2010</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>13012</s2>
<s5>354000190030950240</s5>
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<fA44><s0>0000</s0>
<s1>© 2010 INIST-CNRS. All rights reserved.</s1>
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<fA47 i1="01" i2="1"><s0>10-0128283</s0>
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<fA64 i1="01" i2="1"><s0>Diabetologia : (Berlin)</s0>
</fA64>
<fA66 i1="01"><s0>DEU</s0>
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<fC01 i1="01" l="ENG"><s0>Aims/hypothesis Most of the known actions of angiotensin II have been considered primarily to be the result of angiotensin II subtype 1 receptor activation. However, recent data suggest that the angiotensin II subtype 2 receptor (AT<sub>2</sub>
R) may modulate key processes linked to atherosclerosis. The aim of this study was to investigate the role of AT<sub>2</sub>
R in diabetes-associated atherosclerosis using pharmacological blockade and genetic deficiency. Methods Aortic plaque deposition was assessed in streptozotocin-induced diabetic apolipoprotein E (Apoe) knockout (KO) and At<sub>2</sub>
r (also known as Agtr2)/Apoe double-KO (DKO) mice. Control and diabetic Apoe-KO mice received an AT<sub>2</sub>
R antagonist PD123319 (5 mg kg<sup>-1</sup>
 day<sup>-1</sup>
) via osmotic minipump for 20 weeks (n=7-8 per group). Results Diabetes was associated with a sixfold increase in plaque area (diabetic Apoe-KO: 12.7±1.4% vs control Apoe-KO: 2.3±0.4%, p<0.001) as well as a significant increase in aortic expression of the gene At<sub>2</sub>
r (also known as Agtr2). The increase in plaque area with diabetes was attenuated in AT<sub>2</sub>
R antagonist-treated diabetic Apoe-KO mice (7.1±0.5%, p<0.05) and in diabetic At<sub>2</sub>
r/Apoe DKO mice (9.2±1.3%, p<0.05). These benefits occurred independently of glycaemic control or BP, and were associated with downregulation of a range of pro-inflammatory cytokines, adhesion molecules, chemokines and various extracellular matrix proteins. Conclusionslinterpretation This study provides evidence for AT<sub>2</sub>
R playing a role in the development of diabetes-associated atherosclerosis. These findings suggest a potential utility of AT<sub>2</sub>
R blockers in the prevention and treatment of diabetic macrovascular complications.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B21E01A</s0>
</fC02>
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<fC03 i1="01" i2="X" l="FRE"><s0>Angiotensine II</s0>
<s2>FR</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Angiotensin II</s0>
<s2>FR</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Angiotensina II</s0>
<s2>FR</s2>
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<s5>02</s5>
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<s5>03</s5>
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<s5>07</s5>
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<fC03 i1="05" i2="X" l="ENG"><s0>Development</s0>
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<s5>08</s5>
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<fC03 i1="07" i2="X" l="FRE"><s0>Athérosclérose</s0>
<s2>NM</s2>
<s5>09</s5>
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<s2>NM</s2>
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<s2>NM</s2>
<s5>12</s5>
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<fC03 i1="10" i2="X" l="FRE"><s0>Modèle animal</s0>
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<s2>NS</s2>
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<fC07 i1="07" i2="X" l="SPA"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
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<s2>NS</s2>
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<fC07 i1="08" i2="X" l="ENG"><s0>Mammalia</s0>
<s2>NS</s2>
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<server><NO>PASCAL 10-0128283 INIST</NO>
<ET>Angiotensin II subtype 2 receptor blockade and deficiency attenuate the development of atherosclerosis in an apolipoprotein E-deficient mouse model of diabetes</ET>
<AU>KOÏTKA (A.); CAO (Z.); KOH (P.); WATSON (A. M. D.); SOURRIS (K. C.); LOUFRANI (L.); SORO-PAAVONEN (A.); WALTHER (T.); WOOLLARD (K. J.); JANDELEIT-DAHM (K. A. M.); COOPER (M. E.); ALLEN (T. J.)</AU>
<AF>JDRF Danielle Alberti Memorial Centre for Diabetic Complications, Diabetes Division, Baker IDI Heart and Diabetes Research Institute, PO Box 6492, St Kilda Road Central/Melbourne, VIC 8008/Australie (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 7 aut., 10 aut., 11 aut., 12 aut.); Department of Integrated Neurovascular Biology, University of Angers/Angers/France (6 aut.); Department of Biomedical Sciences, Hull York Medical School, University of Hull/Hull/Royaume-Uni (8 aut.); Vascular Pharmacology, Baker IDI Heart and Diabetes Institute/Melbourne, VIC/Australie (9 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Diabetologia : (Berlin); ISSN 0012-186X; Allemagne; Da. 2010; Vol. 53; No. 3; Pp. 584-592; Bibl. 47 ref.</SO>
<LA>Anglais</LA>
<EA>Aims/hypothesis Most of the known actions of angiotensin II have been considered primarily to be the result of angiotensin II subtype 1 receptor activation. However, recent data suggest that the angiotensin II subtype 2 receptor (AT<sub>2</sub>
R) may modulate key processes linked to atherosclerosis. The aim of this study was to investigate the role of AT<sub>2</sub>
R in diabetes-associated atherosclerosis using pharmacological blockade and genetic deficiency. Methods Aortic plaque deposition was assessed in streptozotocin-induced diabetic apolipoprotein E (Apoe) knockout (KO) and At<sub>2</sub>
r (also known as Agtr2)/Apoe double-KO (DKO) mice. Control and diabetic Apoe-KO mice received an AT<sub>2</sub>
R antagonist PD123319 (5 mg kg<sup>-1</sup>
 day<sup>-1</sup>
) via osmotic minipump for 20 weeks (n=7-8 per group). Results Diabetes was associated with a sixfold increase in plaque area (diabetic Apoe-KO: 12.7±1.4% vs control Apoe-KO: 2.3±0.4%, p<0.001) as well as a significant increase in aortic expression of the gene At<sub>2</sub>
r (also known as Agtr2). The increase in plaque area with diabetes was attenuated in AT<sub>2</sub>
R antagonist-treated diabetic Apoe-KO mice (7.1±0.5%, p<0.05) and in diabetic At<sub>2</sub>
r/Apoe DKO mice (9.2±1.3%, p<0.05). These benefits occurred independently of glycaemic control or BP, and were associated with downregulation of a range of pro-inflammatory cytokines, adhesion molecules, chemokines and various extracellular matrix proteins. Conclusionslinterpretation This study provides evidence for AT<sub>2</sub>
R playing a role in the development of diabetes-associated atherosclerosis. These findings suggest a potential utility of AT<sub>2</sub>
R blockers in the prevention and treatment of diabetic macrovascular complications.</EA>
<CC>002B21E01A; 002B12B01</CC>
<FD>Angiotensine II; Soustype; Récepteur biologique; Déficit; Développement; Apolipoprotéine E; Athérosclérose; Animal; Diabète; Modèle animal; Souris</FD>
<FG>Hormone peptide; Octapeptide; Système renin angiotensine; Pathologie de l'appareil circulatoire; Pathologie des vaisseaux sanguins; Endocrinopathie; Rodentia; Mammalia; Vertebrata</FG>
<ED>Angiotensin II; Subtype; Biological receptor; Deficiency; Development; Apolipoprotein E; Atherosclerosis; Animal; Diabetes mellitus; Animal model; Mouse</ED>
<EG>Peptide hormone; Octapeptide; Renin angiotensin system; Cardiovascular disease; Vascular disease; Endocrinopathy; Rodentia; Mammalia; Vertebrata</EG>
<SD>Angiotensina II; Subtipo; Receptor biológico; Déficiencia; Desarrollo; Apolipoproteína E; Ateroesclerosis; Animal; Diabetes; Modelo animal; Ratón</SD>
<LO>INIST-13012.354000190030950240</LO>
<ID>10-0128283</ID>
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Angiotensin II subtype 2 receptor blockade and deficiency attenuate the development of atherosclerosis in an apolipoprotein E-deficient mouse model of diabetes

Angiotensin II subtype 2 receptor blockade and deficiency attenuate the development of atherosclerosis in an apolipoprotein E-deficient mouse model of diabetes

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