AustralieFrV1, PascalFrancis, Corpus, bibRecord, 002328

Glucocorticoid-Induced Leucine Zipper Is an Endogenous Antiinflammatory Mediator in Arthritis

Identifieur interne : 002328 ( PascalFrancis/Corpus ); précédent : 002327; suivant : 002329

Glucocorticoid-Induced Leucine Zipper Is an Endogenous Antiinflammatory Mediator in Arthritis

Auteurs : Elaine Beaulieu ; Devi Ngo ; Leilani Santos ; YUAN HANG YANG ; Malcolm Smith ; Christian Jorgensen ; Virginie Escriou ; Daniel Scherman ; Gabriel Courties ; Florence Apparailly ; Eric F. Morand

Source :

Arthritis and rheumatism [ 0004-3591 ] ; 2010.

RBID : Pascal:10-0452676

Descripteurs français

Pascal (Inist)
- Leucine, Glucocorticoïde, Antiinflammatoire, Arthrite, Rhumatologie.

English descriptors

KwdEn :
- Antiinflammatory agent, Arthritis, Glucocorticoid, Leucine, Rheumatology.

Abstract

Objective. Glucocorticoid-induced leucine zipper (GILZ) is a glueocorticoid-induced protein, the reported molecular interactions of which suggest that it functions to inhibit inflammation. However, the role of endogenous GILZ in the regulation of inflammation in vivo has not been established. This study was undertaken to examine the expression and function of GILZ in vivo in collagen-induced arthritis (CIA), a murine model of rheumatoid arthritis (RA), and in RA synoviocytes. Methods. GILZ expression was detected in mouse and human synovium by immunohistochemistry and in cultured cells by real-time polymerase chain reaction and permeabilization flow cytometry. GILZ function was assessed in vivo by small interfering RNA (siRNA) silencing using cationic liposome-encapsulated GILZ or control nontargeting siRNA and was assessed in vitro using transient overexpression. Results. GILZ was readily detectable in the synovium of mice with CIA and was up-regulated by therapeutic doses of glucocorticoids. Depleting GILZ expression in vivo increased the clinical and histologic severity of CIA and increased synovial expression of tumor necrosis factor and interleukin-1 (IL-1), without affecting the levels of circulating cytokines or anticollagen antibodies. GILZ was highly expressed in the synovium of patients with active RA and in cultured RA synovial fibroblasts, and GILZ overexpression in synovial fibroblasts inhibited IL-6 and IL-8 release. Conclusion. Our findings indicate that GILZ functions as an endogenous inhibitor of chronic inflammation via effects on cytokine expression and suggest that local modulation of GILZ expression could be a beneficial therapeutic strategy.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

A01	`01`	`1`		`@0 0004-3591`
A02	`01`			`@0 ARHEAW`
A03		`1`		`@0 Arthritis rheum.`
A05				`@2 62`
A06				`@2 9`
A08	`01`	`1`	`ENG`	`@1 Glucocorticoid-Induced Leucine Zipper Is an Endogenous Antiinflammatory Mediator in Arthritis`
A11	`01`	`1`		`@1 BEAULIEU (Elaine)`
A11	`02`	`1`		`@1 NGO (Devi)`
A11	`03`	`1`		`@1 SANTOS (Leilani)`
A11	`04`	`1`		`@1 YUAN HANG YANG`
A11	`05`	`1`		`@1 SMITH (Malcolm)`
A11	`06`	`1`		`@1 JORGENSEN (Christian)`
A11	`07`	`1`		`@1 ESCRIOU (Virginie)`
A11	`08`	`1`		`@1 SCHERMAN (Daniel)`
A11	`09`	`1`		`@1 COURTIES (Gabriel)`
A11	`10`	`1`		`@1 APPARAILLY (Florence)`
A11	`11`	`1`		`@1 MORAND (Eric F.)`
A14	`01`			`@1 Monash Medical Centre and Monash University @2 Melbourne, Victoria @3 AUS @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. @Z 11 aut.`
A14	`02`			`@1 Repatriation General Hospital @2 Adelaide, South Australia @3 AUS @Z 5 aut.`
A14	`03`			`@1 INSERM, U 844, Hôpital Saint Eloi, Centre Hospitalier Universitaire Lapeyronie, and Université Montpellier 1 @2 Montpellier @3 FRA @Z 6 aut. @Z 10 aut.`
A14	`04`			`@1 INSERM, U 640, CNRS, UMR 8151, Université Paris Descartes, and École Nationale Supérieure de Chimie de Paris @2 Paris @3 FRA @Z 7 aut. @Z 8 aut.`
A14	`05`			`@1 INSERM, U 844, Hôpital Saint Eloi, and Université Montpellier 1 @2 Montpellier @3 FRA @Z 9 aut.`
A20				`@1 2651-2661`
A21				`@1 2010`
A23	`01`			`@0 ENG`
A43	`01`			`@1 INIST @2 8711 @5 354000194827520120`
A44				`@0 0000 @1 © 2010 INIST-CNRS. All rights reserved.`
A45				`@0 40 ref.`
A47	`01`	`1`		`@0 10-0452676`
A60				`@1 P`
A61				`@0 A`
A64	`01`	`1`		`@0 Arthritis and rheumatism`
A66	`01`			`@0 USA`
C01	`01`		`ENG`	@0 Objective. Glucocorticoid-induced leucine zipper (GILZ) is a glueocorticoid-induced protein, the reported molecular interactions of which suggest that it functions to inhibit inflammation. However, the role of endogenous GILZ in the regulation of inflammation in vivo has not been established. This study was undertaken to examine the expression and function of GILZ in vivo in collagen-induced arthritis (CIA), a murine model of rheumatoid arthritis (RA), and in RA synoviocytes. Methods. GILZ expression was detected in mouse and human synovium by immunohistochemistry and in cultured cells by real-time polymerase chain reaction and permeabilization flow cytometry. GILZ function was assessed in vivo by small interfering RNA (siRNA) silencing using cationic liposome-encapsulated GILZ or control nontargeting siRNA and was assessed in vitro using transient overexpression. Results. GILZ was readily detectable in the synovium of mice with CIA and was up-regulated by therapeutic doses of glucocorticoids. Depleting GILZ expression in vivo increased the clinical and histologic severity of CIA and increased synovial expression of tumor necrosis factor and interleukin-1 (IL-1), without affecting the levels of circulating cytokines or anticollagen antibodies. GILZ was highly expressed in the synovium of patients with active RA and in cultured RA synovial fibroblasts, and GILZ overexpression in synovial fibroblasts inhibited IL-6 and IL-8 release. Conclusion. Our findings indicate that GILZ functions as an endogenous inhibitor of chronic inflammation via effects on cytokine expression and suggest that local modulation of GILZ expression could be a beneficial therapeutic strategy.
C02	`01`	`X`		`@0 002B15I`
C02	`02`	`X`		`@0 002B02L`
C03	`01`	`X`	`FRE`	`@0 Leucine @2 NK @2 FR @5 04`
C03	`01`	`X`	`ENG`	`@0 Leucine @2 NK @2 FR @5 04`
C03	`01`	`X`	`SPA`	`@0 Leucina @2 NK @2 FR @5 04`
C03	`02`	`X`	`FRE`	`@0 Glucocorticoïde @5 07`
C03	`02`	`X`	`ENG`	`@0 Glucocorticoid @5 07`
C03	`02`	`X`	`SPA`	`@0 Glucocorticoide @5 07`
C03	`03`	`X`	`FRE`	`@0 Antiinflammatoire @5 08`
C03	`03`	`X`	`ENG`	`@0 Antiinflammatory agent @5 08`
C03	`03`	`X`	`SPA`	`@0 Antiinflamatorio @5 08`
C03	`04`	`X`	`FRE`	`@0 Arthrite @5 09`
C03	`04`	`X`	`ENG`	`@0 Arthritis @5 09`
C03	`04`	`X`	`SPA`	`@0 Artritis @5 09`
C03	`05`	`X`	`FRE`	`@0 Rhumatologie @5 13`
C03	`05`	`X`	`ENG`	`@0 Rheumatology @5 13`
C03	`05`	`X`	`SPA`	`@0 Reumatología @5 13`
C07	`01`	`X`	`FRE`	`@0 Pathologie du système ostéoarticulaire @5 37`
C07	`01`	`X`	`ENG`	`@0 Diseases of the osteoarticular system @5 37`
C07	`01`	`X`	`SPA`	`@0 Sistema osteoarticular patología @5 37`
N21				`@1 291`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

Format Inist (serveur)

NO :	PASCAL 10-0452676 INIST
ET :	Glucocorticoid-Induced Leucine Zipper Is an Endogenous Antiinflammatory Mediator in Arthritis
AU :	BEAULIEU (Elaine); NGO (Devi); SANTOS (Leilani); YUAN HANG YANG; SMITH (Malcolm); JORGENSEN (Christian); ESCRIOU (Virginie); SCHERMAN (Daniel); COURTIES (Gabriel); APPARAILLY (Florence); MORAND (Eric F.)
AF :	Monash Medical Centre and Monash University/Melbourne, Victoria/Australie (1 aut., 2 aut., 3 aut., 4 aut., 11 aut.); Repatriation General Hospital/Adelaide, South Australia/Australie (5 aut.); INSERM, U 844, Hôpital Saint Eloi, Centre Hospitalier Universitaire Lapeyronie, and Université Montpellier 1/Montpellier/France (6 aut., 10 aut.); INSERM, U 640, CNRS, UMR 8151, Université Paris Descartes, and École Nationale Supérieure de Chimie de Paris/Paris/France (7 aut., 8 aut.); INSERM, U 844, Hôpital Saint Eloi, and Université Montpellier 1/Montpellier/France (9 aut.)
DT :	Publication en série; Niveau analytique
SO :	Arthritis and rheumatism; ISSN 0004-3591; Coden ARHEAW; Etats-Unis; Da. 2010; Vol. 62; No. 9; Pp. 2651-2661; Bibl. 40 ref.
LA :	Anglais
EA :	Objective. Glucocorticoid-induced leucine zipper (GILZ) is a glueocorticoid-induced protein, the reported molecular interactions of which suggest that it functions to inhibit inflammation. However, the role of endogenous GILZ in the regulation of inflammation in vivo has not been established. This study was undertaken to examine the expression and function of GILZ in vivo in collagen-induced arthritis (CIA), a murine model of rheumatoid arthritis (RA), and in RA synoviocytes. Methods. GILZ expression was detected in mouse and human synovium by immunohistochemistry and in cultured cells by real-time polymerase chain reaction and permeabilization flow cytometry. GILZ function was assessed in vivo by small interfering RNA (siRNA) silencing using cationic liposome-encapsulated GILZ or control nontargeting siRNA and was assessed in vitro using transient overexpression. Results. GILZ was readily detectable in the synovium of mice with CIA and was up-regulated by therapeutic doses of glucocorticoids. Depleting GILZ expression in vivo increased the clinical and histologic severity of CIA and increased synovial expression of tumor necrosis factor and interleukin-1 (IL-1), without affecting the levels of circulating cytokines or anticollagen antibodies. GILZ was highly expressed in the synovium of patients with active RA and in cultured RA synovial fibroblasts, and GILZ overexpression in synovial fibroblasts inhibited IL-6 and IL-8 release. Conclusion. Our findings indicate that GILZ functions as an endogenous inhibitor of chronic inflammation via effects on cytokine expression and suggest that local modulation of GILZ expression could be a beneficial therapeutic strategy.
CC :	002B15I; 002B02L
FD :	Leucine; Glucocorticoïde; Antiinflammatoire; Arthrite; Rhumatologie
FG :	Pathologie du système ostéoarticulaire
ED :	Leucine; Glucocorticoid; Antiinflammatory agent; Arthritis; Rheumatology
EG :	Diseases of the osteoarticular system
SD :	Leucina; Glucocorticoide; Antiinflamatorio; Artritis; Reumatología
LO :	INIST-8711.354000194827520120
ID :	10-0452676

Links to Exploration step

Pascal:10-0452676

Le document en format XML

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<author><name sortKey="Yuan Hang Yang" sort="Yuan Hang Yang" uniqKey="Yuan Hang Yang" last="Yuan Hang Yang">YUAN HANG YANG</name>
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<author><name sortKey="Escriou, Virginie" sort="Escriou, Virginie" uniqKey="Escriou V" first="Virginie" last="Escriou">Virginie Escriou</name>
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<author><name sortKey="Courties, Gabriel" sort="Courties, Gabriel" uniqKey="Courties G" first="Gabriel" last="Courties">Gabriel Courties</name>
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<author><name sortKey="Apparailly, Florence" sort="Apparailly, Florence" uniqKey="Apparailly F" first="Florence" last="Apparailly">Florence Apparailly</name>
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<series><title level="j" type="main">Arthritis and rheumatism</title>
<title level="j" type="abbreviated">Arthritis rheum.</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antiinflammatory agent</term>
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<keywords scheme="Pascal" xml:lang="fr"><term>Leucine</term>
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<front><div type="abstract" xml:lang="en">Objective. Glucocorticoid-induced leucine zipper (GILZ) is a glueocorticoid-induced protein, the reported molecular interactions of which suggest that it functions to inhibit inflammation. However, the role of endogenous GILZ in the regulation of inflammation in vivo has not been established. This study was undertaken to examine the expression and function of GILZ in vivo in collagen-induced arthritis (CIA), a murine model of rheumatoid arthritis (RA), and in RA synoviocytes. Methods. GILZ expression was detected in mouse and human synovium by immunohistochemistry and in cultured cells by real-time polymerase chain reaction and permeabilization flow cytometry. GILZ function was assessed in vivo by small interfering RNA (siRNA) silencing using cationic liposome-encapsulated GILZ or control nontargeting siRNA and was assessed in vitro using transient overexpression. Results. GILZ was readily detectable in the synovium of mice with CIA and was up-regulated by therapeutic doses of glucocorticoids. Depleting GILZ expression in vivo increased the clinical and histologic severity of CIA and increased synovial expression of tumor necrosis factor and interleukin-1 (IL-1), without affecting the levels of circulating cytokines or anticollagen antibodies. GILZ was highly expressed in the synovium of patients with active RA and in cultured RA synovial fibroblasts, and GILZ overexpression in synovial fibroblasts inhibited IL-6 and IL-8 release. Conclusion. Our findings indicate that GILZ functions as an endogenous inhibitor of chronic inflammation via effects on cytokine expression and suggest that local modulation of GILZ expression could be a beneficial therapeutic strategy.</div>
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<ET>Glucocorticoid-Induced Leucine Zipper Is an Endogenous Antiinflammatory Mediator in Arthritis</ET>
<AU>BEAULIEU (Elaine); NGO (Devi); SANTOS (Leilani); YUAN HANG YANG; SMITH (Malcolm); JORGENSEN (Christian); ESCRIOU (Virginie); SCHERMAN (Daniel); COURTIES (Gabriel); APPARAILLY (Florence); MORAND (Eric F.)</AU>
<AF>Monash Medical Centre and Monash University/Melbourne, Victoria/Australie (1 aut., 2 aut., 3 aut., 4 aut., 11 aut.); Repatriation General Hospital/Adelaide, South Australia/Australie (5 aut.); INSERM, U 844, Hôpital Saint Eloi, Centre Hospitalier Universitaire Lapeyronie, and Université Montpellier 1/Montpellier/France (6 aut., 10 aut.); INSERM, U 640, CNRS, UMR 8151, Université Paris Descartes, and École Nationale Supérieure de Chimie de Paris/Paris/France (7 aut., 8 aut.); INSERM, U 844, Hôpital Saint Eloi, and Université Montpellier 1/Montpellier/France (9 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Arthritis and rheumatism; ISSN 0004-3591; Coden ARHEAW; Etats-Unis; Da. 2010; Vol. 62; No. 9; Pp. 2651-2661; Bibl. 40 ref.</SO>
<LA>Anglais</LA>
<EA>Objective. Glucocorticoid-induced leucine zipper (GILZ) is a glueocorticoid-induced protein, the reported molecular interactions of which suggest that it functions to inhibit inflammation. However, the role of endogenous GILZ in the regulation of inflammation in vivo has not been established. This study was undertaken to examine the expression and function of GILZ in vivo in collagen-induced arthritis (CIA), a murine model of rheumatoid arthritis (RA), and in RA synoviocytes. Methods. GILZ expression was detected in mouse and human synovium by immunohistochemistry and in cultured cells by real-time polymerase chain reaction and permeabilization flow cytometry. GILZ function was assessed in vivo by small interfering RNA (siRNA) silencing using cationic liposome-encapsulated GILZ or control nontargeting siRNA and was assessed in vitro using transient overexpression. Results. GILZ was readily detectable in the synovium of mice with CIA and was up-regulated by therapeutic doses of glucocorticoids. Depleting GILZ expression in vivo increased the clinical and histologic severity of CIA and increased synovial expression of tumor necrosis factor and interleukin-1 (IL-1), without affecting the levels of circulating cytokines or anticollagen antibodies. GILZ was highly expressed in the synovium of patients with active RA and in cultured RA synovial fibroblasts, and GILZ overexpression in synovial fibroblasts inhibited IL-6 and IL-8 release. Conclusion. Our findings indicate that GILZ functions as an endogenous inhibitor of chronic inflammation via effects on cytokine expression and suggest that local modulation of GILZ expression could be a beneficial therapeutic strategy.</EA>
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<FD>Leucine; Glucocorticoïde; Antiinflammatoire; Arthrite; Rhumatologie</FD>
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<SD>Leucina; Glucocorticoide; Antiinflamatorio; Artritis; Reumatología</SD>
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Glucocorticoid-Induced Leucine Zipper Is an Endogenous Antiinflammatory Mediator in Arthritis

Glucocorticoid-Induced Leucine Zipper Is an Endogenous Antiinflammatory Mediator in Arthritis

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