EdenteV2, PascalFrancis, Corpus, bibRecord, 000258

Cyclosporine A enhances apoptosis in gingival keratinocytes of rats and in OECM1 cells via the mitochondrial pathway

Identifieur interne : 000258 ( PascalFrancis/Corpus ); précédent : 000257; suivant : 000259

Cyclosporine A enhances apoptosis in gingival keratinocytes of rats and in OECM1 cells via the mitochondrial pathway

Auteurs : H.-P. Tu ; Y.-T. Chen ; H.-C. Chiu ; Y.-T. Chin ; S.-M. Huang ; L.-C. Cheng ; E. Fu ; C.-Y. Chiang

Source :

Journal of periodontal research [ 0022-3484 ] ; 2009.

RBID : Pascal:09-0450367

Descripteurs français

Pascal (Inist)
- Ciclosporine, Apoptose, Gencive, Kératinocyte, Animal, Rat, Cellule, Stomatologie, Immunodépresseur.

English descriptors

KwdEn :
- Animal, Apoptosis, Cell, Ciclosporin, Gingiva, Immunosuppressive agent, Keratinocyte, Rat, Stomatology.

Abstract

Background and Objective: We reported previously that cyclosporine A induces a high level of expression of p21 in rat gingival keratinocytes and in OECM 1 cells. In this study, the apoptosis of gingival keratinocytes after treatment with cyclosporine A was evaluated using the same models. Material and Methods: Forty Sprague-Dawley rats with right edentulous ridges were assigned into cyclosporine A (30 mg/kg) and control groups. Four weeks later, gingivae were screened for expression of apoptotic genes using microarray analyses and DNA fragmentation. The expression of bcl2-associated X protein (Bax), apoptosis-inducing factor (AIF) and Caspase 3 mRNAs, and the expression of Bax, AIF, Caspase 9 and Fas proteins, were analyzed using the reverse transcription-polymerase chain reaction and immunohistochemistry, respectively. Apoptosis in OECM 1 cells (keratinocytes of a gingival carcinoma cell line), after treatment with cyclosporine A, was evaluated by 4',6-diamidino-2-phenylindole (DAPI) staining and flow cytometry, whereas the expression of Bax, AIF, Caspase 3 and 8, Bcl-2 and Fas proteins were examined using western blotting. Results: According to microarray analyses, the expression of certain apoptotic genes was altered in the gingiva of rats who received cyclosporine A, and increased number of DNA fragments were detected. Expression of mRNA or protein for Bax, AIF and Caspase 3 and 9 in the gingivae of rats increased after treatment with cyclosporine A. An increased number of apoptotic bodies and of OECM 1 cells in the sub-G1 phase was observed after treatment with cyclosporine A. Increased expression of AIF, Bax and Caspase 3 protein, but not of bcl-2, Caspase 8 or Fas protein, was observed in cells after treatment with cyclosporine A. Conclusion: Based on the above findings, we suggest that cyclosporine A might enhance the apoptosis of gingival keratinocytes, mainly via the mitochondrial pathway.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

A01	`01`	`1`		`@0 0022-3484`
A03		`1`		`@0 J. periodontal res.`
A05				`@2 44`
A06				`@2 6`
A08	`01`	`1`	`ENG`	`@1 Cyclosporine A enhances apoptosis in gingival keratinocytes of rats and in OECM1 cells via the mitochondrial pathway`
A11	`01`	`1`		`@1 TU (H.-P.)`
A11	`02`	`1`		`@1 CHEN (Y.-T.)`
A11	`03`	`1`		`@1 CHIU (H.-C.)`
A11	`04`	`1`		`@1 CHIN (Y.-T.)`
A11	`05`	`1`		`@1 HUANG (S.-M.)`
A11	`06`	`1`		`@1 CHENG (L.-C.)`
A11	`07`	`1`		`@1 FU (E.)`
A11	`08`	`1`		`@1 CHIANG (C.-Y.)`
A14	`01`			`@1 Department of Periodontology, School of Dentistry, National Defense Medical Center and Tri-Service General Hospital @2 Taipei @3 TWN @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. @Z 7 aut. @Z 8 aut.`
A14	`02`			`@1 Department of Dental Hygiene, China Medical University @2 Taichung @3 TWN @Z 1 aut.`
A14	`03`			`@1 Department of Biochemistry, National Defense Medical Center @2 Taipei @3 TWN @Z 5 aut.`
A14	`04`			`@1 Department of Internal Medicine, School of Medicine, Chang Gung University @2 Taipei Country @3 TWN @Z 6 aut.`
A20				`@1 767-775`
A21				`@1 2009`
A23	`01`			`@0 ENG`
A43	`01`			`@1 INIST @2 15072 @5 354000170114540110`
A44				`@0 0000 @1 © 2009 INIST-CNRS. All rights reserved.`
A45				`@0 47 ref.`
A47	`01`	`1`		`@0 09-0450367`
A60				`@1 P`
A61				`@0 A`
A64	`01`	`1`		`@0 Journal of periodontal research`
A66	`01`			`@0 GBR`
C01	`01`		`ENG`	@0 Background and Objective: We reported previously that cyclosporine A induces a high level of expression of p21 in rat gingival keratinocytes and in OECM 1 cells. In this study, the apoptosis of gingival keratinocytes after treatment with cyclosporine A was evaluated using the same models. Material and Methods: Forty Sprague-Dawley rats with right edentulous ridges were assigned into cyclosporine A (30 mg/kg) and control groups. Four weeks later, gingivae were screened for expression of apoptotic genes using microarray analyses and DNA fragmentation. The expression of bcl2-associated X protein (Bax), apoptosis-inducing factor (AIF) and Caspase 3 mRNAs, and the expression of Bax, AIF, Caspase 9 and Fas proteins, were analyzed using the reverse transcription-polymerase chain reaction and immunohistochemistry, respectively. Apoptosis in OECM 1 cells (keratinocytes of a gingival carcinoma cell line), after treatment with cyclosporine A, was evaluated by 4',6-diamidino-2-phenylindole (DAPI) staining and flow cytometry, whereas the expression of Bax, AIF, Caspase 3 and 8, Bcl-2 and Fas proteins were examined using western blotting. Results: According to microarray analyses, the expression of certain apoptotic genes was altered in the gingiva of rats who received cyclosporine A, and increased number of DNA fragments were detected. Expression of mRNA or protein for Bax, AIF and Caspase 3 and 9 in the gingivae of rats increased after treatment with cyclosporine A. An increased number of apoptotic bodies and of OECM 1 cells in the sub-G1 phase was observed after treatment with cyclosporine A. Increased expression of AIF, Bax and Caspase 3 protein, but not of bcl-2, Caspase 8 or Fas protein, was observed in cells after treatment with cyclosporine A. Conclusion: Based on the above findings, we suggest that cyclosporine A might enhance the apoptosis of gingival keratinocytes, mainly via the mitochondrial pathway.
C02	`01`	`X`		`@0 002B10`
C03	`01`	`X`	`FRE`	`@0 Ciclosporine @2 NK @2 FR @5 04`
C03	`01`	`X`	`ENG`	`@0 Ciclosporin @2 NK @2 FR @5 04`
C03	`01`	`X`	`SPA`	`@0 Ciclosporina @2 NK @2 FR @5 04`
C03	`02`	`X`	`FRE`	`@0 Apoptose @5 07`
C03	`02`	`X`	`ENG`	`@0 Apoptosis @5 07`
C03	`02`	`X`	`SPA`	`@0 Apoptosis @5 07`
C03	`03`	`X`	`FRE`	`@0 Gencive @5 08`
C03	`03`	`X`	`ENG`	`@0 Gingiva @5 08`
C03	`03`	`X`	`SPA`	`@0 Encía @5 08`
C03	`04`	`X`	`FRE`	`@0 Kératinocyte @5 09`
C03	`04`	`X`	`ENG`	`@0 Keratinocyte @5 09`
C03	`04`	`X`	`SPA`	`@0 Queratinocito @5 09`
C03	`05`	`X`	`FRE`	`@0 Animal @5 13`
C03	`05`	`X`	`ENG`	`@0 Animal @5 13`
C03	`05`	`X`	`SPA`	`@0 Animal @5 13`
C03	`06`	`X`	`FRE`	`@0 Rat @5 14`
C03	`06`	`X`	`ENG`	`@0 Rat @5 14`
C03	`06`	`X`	`SPA`	`@0 Rata @5 14`
C03	`07`	`X`	`FRE`	`@0 Cellule @5 15`
C03	`07`	`X`	`ENG`	`@0 Cell @5 15`
C03	`07`	`X`	`SPA`	`@0 Célula @5 15`
C03	`08`	`X`	`FRE`	`@0 Stomatologie @5 16`
C03	`08`	`X`	`ENG`	`@0 Stomatology @5 16`
C03	`08`	`X`	`SPA`	`@0 Estomatología @5 16`
C03	`09`	`X`	`FRE`	`@0 Immunodépresseur @5 30`
C03	`09`	`X`	`ENG`	`@0 Immunosuppressive agent @5 30`
C03	`09`	`X`	`SPA`	`@0 Inmunodepresor @5 30`
C07	`01`	`X`	`FRE`	`@0 Rodentia @2 NS`
C07	`01`	`X`	`ENG`	`@0 Rodentia @2 NS`
C07	`01`	`X`	`SPA`	`@0 Rodentia @2 NS`
C07	`02`	`X`	`FRE`	`@0 Mammalia @2 NS`
C07	`02`	`X`	`ENG`	`@0 Mammalia @2 NS`
C07	`02`	`X`	`SPA`	`@0 Mammalia @2 NS`
C07	`03`	`X`	`FRE`	`@0 Vertebrata @2 NS`
C07	`03`	`X`	`ENG`	`@0 Vertebrata @2 NS`
C07	`03`	`X`	`SPA`	`@0 Vertebrata @2 NS`
N21				`@1 327`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

Format Inist (serveur)

NO :	PASCAL 09-0450367 INIST
ET :	Cyclosporine A enhances apoptosis in gingival keratinocytes of rats and in OECM1 cells via the mitochondrial pathway
AU :	TU (H.-P.); CHEN (Y.-T.); CHIU (H.-C.); CHIN (Y.-T.); HUANG (S.-M.); CHENG (L.-C.); FU (E.); CHIANG (C.-Y.)
AF :	Department of Periodontology, School of Dentistry, National Defense Medical Center and Tri-Service General Hospital/Taipei/Taïwan (1 aut., 2 aut., 3 aut., 4 aut., 7 aut., 8 aut.); Department of Dental Hygiene, China Medical University/Taichung/Taïwan (1 aut.); Department of Biochemistry, National Defense Medical Center/Taipei/Taïwan (5 aut.); Department of Internal Medicine, School of Medicine, Chang Gung University/Taipei Country/Taïwan (6 aut.)
DT :	Publication en série; Niveau analytique
SO :	Journal of periodontal research; ISSN 0022-3484; Royaume-Uni; Da. 2009; Vol. 44; No. 6; Pp. 767-775; Bibl. 47 ref.
LA :	Anglais
EA :	Background and Objective: We reported previously that cyclosporine A induces a high level of expression of p21 in rat gingival keratinocytes and in OECM 1 cells. In this study, the apoptosis of gingival keratinocytes after treatment with cyclosporine A was evaluated using the same models. Material and Methods: Forty Sprague-Dawley rats with right edentulous ridges were assigned into cyclosporine A (30 mg/kg) and control groups. Four weeks later, gingivae were screened for expression of apoptotic genes using microarray analyses and DNA fragmentation. The expression of bcl2-associated X protein (Bax), apoptosis-inducing factor (AIF) and Caspase 3 mRNAs, and the expression of Bax, AIF, Caspase 9 and Fas proteins, were analyzed using the reverse transcription-polymerase chain reaction and immunohistochemistry, respectively. Apoptosis in OECM 1 cells (keratinocytes of a gingival carcinoma cell line), after treatment with cyclosporine A, was evaluated by 4',6-diamidino-2-phenylindole (DAPI) staining and flow cytometry, whereas the expression of Bax, AIF, Caspase 3 and 8, Bcl-2 and Fas proteins were examined using western blotting. Results: According to microarray analyses, the expression of certain apoptotic genes was altered in the gingiva of rats who received cyclosporine A, and increased number of DNA fragments were detected. Expression of mRNA or protein for Bax, AIF and Caspase 3 and 9 in the gingivae of rats increased after treatment with cyclosporine A. An increased number of apoptotic bodies and of OECM 1 cells in the sub-G1 phase was observed after treatment with cyclosporine A. Increased expression of AIF, Bax and Caspase 3 protein, but not of bcl-2, Caspase 8 or Fas protein, was observed in cells after treatment with cyclosporine A. Conclusion: Based on the above findings, we suggest that cyclosporine A might enhance the apoptosis of gingival keratinocytes, mainly via the mitochondrial pathway.
CC :	002B10
FD :	Ciclosporine; Apoptose; Gencive; Kératinocyte; Animal; Rat; Cellule; Stomatologie; Immunodépresseur
FG :	Rodentia; Mammalia; Vertebrata
ED :	Ciclosporin; Apoptosis; Gingiva; Keratinocyte; Animal; Rat; Cell; Stomatology; Immunosuppressive agent
EG :	Rodentia; Mammalia; Vertebrata
SD :	Ciclosporina; Apoptosis; Encía; Queratinocito; Animal; Rata; Célula; Estomatología; Inmunodepresor
LO :	INIST-15072.354000170114540110
ID :	09-0450367

Links to Exploration step

Pascal:09-0450367

Le document en format XML

<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">Cyclosporine A enhances apoptosis in gingival keratinocytes of rats and in OECM1 cells via the mitochondrial pathway</title>
<author><name sortKey="Tu, H P" sort="Tu, H P" uniqKey="Tu H" first="H.-P." last="Tu">H.-P. Tu</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Periodontology, School of Dentistry, National Defense Medical Center and Tri-Service General Hospital</s1>
<s2>Taipei</s2>
<s3>TWN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Department of Dental Hygiene, China Medical University</s1>
<s2>Taichung</s2>
<s3>TWN</s3>
<sZ>1 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Chen, Y T" sort="Chen, Y T" uniqKey="Chen Y" first="Y.-T." last="Chen">Y.-T. Chen</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Periodontology, School of Dentistry, National Defense Medical Center and Tri-Service General Hospital</s1>
<s2>Taipei</s2>
<s3>TWN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Chiu, H C" sort="Chiu, H C" uniqKey="Chiu H" first="H.-C." last="Chiu">H.-C. Chiu</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Periodontology, School of Dentistry, National Defense Medical Center and Tri-Service General Hospital</s1>
<s2>Taipei</s2>
<s3>TWN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Chin, Y T" sort="Chin, Y T" uniqKey="Chin Y" first="Y.-T." last="Chin">Y.-T. Chin</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Periodontology, School of Dentistry, National Defense Medical Center and Tri-Service General Hospital</s1>
<s2>Taipei</s2>
<s3>TWN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Huang, S M" sort="Huang, S M" uniqKey="Huang S" first="S.-M." last="Huang">S.-M. Huang</name>
<affiliation><inist:fA14 i1="03"><s1>Department of Biochemistry, National Defense Medical Center</s1>
<s2>Taipei</s2>
<s3>TWN</s3>
<sZ>5 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Cheng, L C" sort="Cheng, L C" uniqKey="Cheng L" first="L.-C." last="Cheng">L.-C. Cheng</name>
<affiliation><inist:fA14 i1="04"><s1>Department of Internal Medicine, School of Medicine, Chang Gung University</s1>
<s2>Taipei Country</s2>
<s3>TWN</s3>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Fu, E" sort="Fu, E" uniqKey="Fu E" first="E." last="Fu">E. Fu</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Periodontology, School of Dentistry, National Defense Medical Center and Tri-Service General Hospital</s1>
<s2>Taipei</s2>
<s3>TWN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Chiang, C Y" sort="Chiang, C Y" uniqKey="Chiang C" first="C.-Y." last="Chiang">C.-Y. Chiang</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Periodontology, School of Dentistry, National Defense Medical Center and Tri-Service General Hospital</s1>
<s2>Taipei</s2>
<s3>TWN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">INIST</idno>
<idno type="inist">09-0450367</idno>
<date when="2009">2009</date>
<idno type="stanalyst">PASCAL 09-0450367 INIST</idno>
<idno type="RBID">Pascal:09-0450367</idno>
<idno type="wicri:Area/PascalFrancis/Corpus">000258</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Cyclosporine A enhances apoptosis in gingival keratinocytes of rats and in OECM1 cells via the mitochondrial pathway</title>
<author><name sortKey="Tu, H P" sort="Tu, H P" uniqKey="Tu H" first="H.-P." last="Tu">H.-P. Tu</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Periodontology, School of Dentistry, National Defense Medical Center and Tri-Service General Hospital</s1>
<s2>Taipei</s2>
<s3>TWN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Department of Dental Hygiene, China Medical University</s1>
<s2>Taichung</s2>
<s3>TWN</s3>
<sZ>1 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Chen, Y T" sort="Chen, Y T" uniqKey="Chen Y" first="Y.-T." last="Chen">Y.-T. Chen</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Periodontology, School of Dentistry, National Defense Medical Center and Tri-Service General Hospital</s1>
<s2>Taipei</s2>
<s3>TWN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Chiu, H C" sort="Chiu, H C" uniqKey="Chiu H" first="H.-C." last="Chiu">H.-C. Chiu</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Periodontology, School of Dentistry, National Defense Medical Center and Tri-Service General Hospital</s1>
<s2>Taipei</s2>
<s3>TWN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Chin, Y T" sort="Chin, Y T" uniqKey="Chin Y" first="Y.-T." last="Chin">Y.-T. Chin</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Periodontology, School of Dentistry, National Defense Medical Center and Tri-Service General Hospital</s1>
<s2>Taipei</s2>
<s3>TWN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Huang, S M" sort="Huang, S M" uniqKey="Huang S" first="S.-M." last="Huang">S.-M. Huang</name>
<affiliation><inist:fA14 i1="03"><s1>Department of Biochemistry, National Defense Medical Center</s1>
<s2>Taipei</s2>
<s3>TWN</s3>
<sZ>5 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Cheng, L C" sort="Cheng, L C" uniqKey="Cheng L" first="L.-C." last="Cheng">L.-C. Cheng</name>
<affiliation><inist:fA14 i1="04"><s1>Department of Internal Medicine, School of Medicine, Chang Gung University</s1>
<s2>Taipei Country</s2>
<s3>TWN</s3>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Fu, E" sort="Fu, E" uniqKey="Fu E" first="E." last="Fu">E. Fu</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Periodontology, School of Dentistry, National Defense Medical Center and Tri-Service General Hospital</s1>
<s2>Taipei</s2>
<s3>TWN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Chiang, C Y" sort="Chiang, C Y" uniqKey="Chiang C" first="C.-Y." last="Chiang">C.-Y. Chiang</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Periodontology, School of Dentistry, National Defense Medical Center and Tri-Service General Hospital</s1>
<s2>Taipei</s2>
<s3>TWN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</analytic>
<series><title level="j" type="main">Journal of periodontal research</title>
<title level="j" type="abbreviated">J. periodontal res.</title>
<idno type="ISSN">0022-3484</idno>
<imprint><date when="2009">2009</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><title level="j" type="main">Journal of periodontal research</title>
<title level="j" type="abbreviated">J. periodontal res.</title>
<idno type="ISSN">0022-3484</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animal</term>
<term>Apoptosis</term>
<term>Cell</term>
<term>Ciclosporin</term>
<term>Gingiva</term>
<term>Immunosuppressive agent</term>
<term>Keratinocyte</term>
<term>Rat</term>
<term>Stomatology</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Ciclosporine</term>
<term>Apoptose</term>
<term>Gencive</term>
<term>Kératinocyte</term>
<term>Animal</term>
<term>Rat</term>
<term>Cellule</term>
<term>Stomatologie</term>
<term>Immunodépresseur</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Background and Objective: We reported previously that cyclosporine A induces a high level of expression of p21 in rat gingival keratinocytes and in OECM 1 cells. In this study, the apoptosis of gingival keratinocytes after treatment with cyclosporine A was evaluated using the same models. Material and Methods: Forty Sprague-Dawley rats with right edentulous ridges were assigned into cyclosporine A (30 mg/kg) and control groups. Four weeks later, gingivae were screened for expression of apoptotic genes using microarray analyses and DNA fragmentation. The expression of bcl2-associated X protein (Bax), apoptosis-inducing factor (AIF) and Caspase 3 mRNAs, and the expression of Bax, AIF, Caspase 9 and Fas proteins, were analyzed using the reverse transcription-polymerase chain reaction and immunohistochemistry, respectively. Apoptosis in OECM 1 cells (keratinocytes of a gingival carcinoma cell line), after treatment with cyclosporine A, was evaluated by 4',6-diamidino-2-phenylindole (DAPI) staining and flow cytometry, whereas the expression of Bax, AIF, Caspase 3 and 8, Bcl-2 and Fas proteins were examined using western blotting. Results: According to microarray analyses, the expression of certain apoptotic genes was altered in the gingiva of rats who received cyclosporine A, and increased number of DNA fragments were detected. Expression of mRNA or protein for Bax, AIF and Caspase 3 and 9 in the gingivae of rats increased after treatment with cyclosporine A. An increased number of apoptotic bodies and of OECM 1 cells in the sub-G1 phase was observed after treatment with cyclosporine A. Increased expression of AIF, Bax and Caspase 3 protein, but not of bcl-2, Caspase 8 or Fas protein, was observed in cells after treatment with cyclosporine A. Conclusion: Based on the above findings, we suggest that cyclosporine A might enhance the apoptosis of gingival keratinocytes, mainly via the mitochondrial pathway.</div>
</front>
</TEI>
<inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0022-3484</s0>
</fA01>
<fA03 i2="1"><s0>J. periodontal res.</s0>
</fA03>
<fA05><s2>44</s2>
</fA05>
<fA06><s2>6</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>Cyclosporine A enhances apoptosis in gingival keratinocytes of rats and in OECM1 cells via the mitochondrial pathway</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>TU (H.-P.)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>CHEN (Y.-T.)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>CHIU (H.-C.)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>CHIN (Y.-T.)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>HUANG (S.-M.)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>CHENG (L.-C.)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>FU (E.)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>CHIANG (C.-Y.)</s1>
</fA11>
<fA14 i1="01"><s1>Department of Periodontology, School of Dentistry, National Defense Medical Center and Tri-Service General Hospital</s1>
<s2>Taipei</s2>
<s3>TWN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>7 aut.</sZ>
<sZ>8 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Department of Dental Hygiene, China Medical University</s1>
<s2>Taichung</s2>
<s3>TWN</s3>
<sZ>1 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Department of Biochemistry, National Defense Medical Center</s1>
<s2>Taipei</s2>
<s3>TWN</s3>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Department of Internal Medicine, School of Medicine, Chang Gung University</s1>
<s2>Taipei Country</s2>
<s3>TWN</s3>
<sZ>6 aut.</sZ>
</fA14>
<fA20><s1>767-775</s1>
</fA20>
<fA21><s1>2009</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>15072</s2>
<s5>354000170114540110</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2009 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>47 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>09-0450367</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Journal of periodontal research</s0>
</fA64>
<fA66 i1="01"><s0>GBR</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>Background and Objective: We reported previously that cyclosporine A induces a high level of expression of p21 in rat gingival keratinocytes and in OECM 1 cells. In this study, the apoptosis of gingival keratinocytes after treatment with cyclosporine A was evaluated using the same models. Material and Methods: Forty Sprague-Dawley rats with right edentulous ridges were assigned into cyclosporine A (30 mg/kg) and control groups. Four weeks later, gingivae were screened for expression of apoptotic genes using microarray analyses and DNA fragmentation. The expression of bcl2-associated X protein (Bax), apoptosis-inducing factor (AIF) and Caspase 3 mRNAs, and the expression of Bax, AIF, Caspase 9 and Fas proteins, were analyzed using the reverse transcription-polymerase chain reaction and immunohistochemistry, respectively. Apoptosis in OECM 1 cells (keratinocytes of a gingival carcinoma cell line), after treatment with cyclosporine A, was evaluated by 4',6-diamidino-2-phenylindole (DAPI) staining and flow cytometry, whereas the expression of Bax, AIF, Caspase 3 and 8, Bcl-2 and Fas proteins were examined using western blotting. Results: According to microarray analyses, the expression of certain apoptotic genes was altered in the gingiva of rats who received cyclosporine A, and increased number of DNA fragments were detected. Expression of mRNA or protein for Bax, AIF and Caspase 3 and 9 in the gingivae of rats increased after treatment with cyclosporine A. An increased number of apoptotic bodies and of OECM 1 cells in the sub-G1 phase was observed after treatment with cyclosporine A. Increased expression of AIF, Bax and Caspase 3 protein, but not of bcl-2, Caspase 8 or Fas protein, was observed in cells after treatment with cyclosporine A. Conclusion: Based on the above findings, we suggest that cyclosporine A might enhance the apoptosis of gingival keratinocytes, mainly via the mitochondrial pathway.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B10</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Ciclosporine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>04</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Ciclosporin</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>04</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Ciclosporina</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>04</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Apoptose</s0>
<s5>07</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Apoptosis</s0>
<s5>07</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Apoptosis</s0>
<s5>07</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Gencive</s0>
<s5>08</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Gingiva</s0>
<s5>08</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Encía</s0>
<s5>08</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Kératinocyte</s0>
<s5>09</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Keratinocyte</s0>
<s5>09</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Queratinocito</s0>
<s5>09</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Animal</s0>
<s5>13</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Animal</s0>
<s5>13</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Animal</s0>
<s5>13</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Rat</s0>
<s5>14</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Rat</s0>
<s5>14</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Rata</s0>
<s5>14</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Cellule</s0>
<s5>15</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Cell</s0>
<s5>15</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Célula</s0>
<s5>15</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Stomatologie</s0>
<s5>16</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Stomatology</s0>
<s5>16</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Estomatología</s0>
<s5>16</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Immunodépresseur</s0>
<s5>30</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Immunosuppressive agent</s0>
<s5>30</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Inmunodepresor</s0>
<s5>30</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fN21><s1>327</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 09-0450367 INIST</NO>
<ET>Cyclosporine A enhances apoptosis in gingival keratinocytes of rats and in OECM1 cells via the mitochondrial pathway</ET>
<AU>TU (H.-P.); CHEN (Y.-T.); CHIU (H.-C.); CHIN (Y.-T.); HUANG (S.-M.); CHENG (L.-C.); FU (E.); CHIANG (C.-Y.)</AU>
<AF>Department of Periodontology, School of Dentistry, National Defense Medical Center and Tri-Service General Hospital/Taipei/Taïwan (1 aut., 2 aut., 3 aut., 4 aut., 7 aut., 8 aut.); Department of Dental Hygiene, China Medical University/Taichung/Taïwan (1 aut.); Department of Biochemistry, National Defense Medical Center/Taipei/Taïwan (5 aut.); Department of Internal Medicine, School of Medicine, Chang Gung University/Taipei Country/Taïwan (6 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Journal of periodontal research; ISSN 0022-3484; Royaume-Uni; Da. 2009; Vol. 44; No. 6; Pp. 767-775; Bibl. 47 ref.</SO>
<LA>Anglais</LA>
<EA>Background and Objective: We reported previously that cyclosporine A induces a high level of expression of p21 in rat gingival keratinocytes and in OECM 1 cells. In this study, the apoptosis of gingival keratinocytes after treatment with cyclosporine A was evaluated using the same models. Material and Methods: Forty Sprague-Dawley rats with right edentulous ridges were assigned into cyclosporine A (30 mg/kg) and control groups. Four weeks later, gingivae were screened for expression of apoptotic genes using microarray analyses and DNA fragmentation. The expression of bcl2-associated X protein (Bax), apoptosis-inducing factor (AIF) and Caspase 3 mRNAs, and the expression of Bax, AIF, Caspase 9 and Fas proteins, were analyzed using the reverse transcription-polymerase chain reaction and immunohistochemistry, respectively. Apoptosis in OECM 1 cells (keratinocytes of a gingival carcinoma cell line), after treatment with cyclosporine A, was evaluated by 4',6-diamidino-2-phenylindole (DAPI) staining and flow cytometry, whereas the expression of Bax, AIF, Caspase 3 and 8, Bcl-2 and Fas proteins were examined using western blotting. Results: According to microarray analyses, the expression of certain apoptotic genes was altered in the gingiva of rats who received cyclosporine A, and increased number of DNA fragments were detected. Expression of mRNA or protein for Bax, AIF and Caspase 3 and 9 in the gingivae of rats increased after treatment with cyclosporine A. An increased number of apoptotic bodies and of OECM 1 cells in the sub-G1 phase was observed after treatment with cyclosporine A. Increased expression of AIF, Bax and Caspase 3 protein, but not of bcl-2, Caspase 8 or Fas protein, was observed in cells after treatment with cyclosporine A. Conclusion: Based on the above findings, we suggest that cyclosporine A might enhance the apoptosis of gingival keratinocytes, mainly via the mitochondrial pathway.</EA>
<CC>002B10</CC>
<FD>Ciclosporine; Apoptose; Gencive; Kératinocyte; Animal; Rat; Cellule; Stomatologie; Immunodépresseur</FD>
<FG>Rodentia; Mammalia; Vertebrata</FG>
<ED>Ciclosporin; Apoptosis; Gingiva; Keratinocyte; Animal; Rat; Cell; Stomatology; Immunosuppressive agent</ED>
<EG>Rodentia; Mammalia; Vertebrata</EG>
<SD>Ciclosporina; Apoptosis; Encía; Queratinocito; Animal; Rata; Célula; Estomatología; Inmunodepresor</SD>
<LO>INIST-15072.354000170114540110</LO>
<ID>09-0450367</ID>
</server>
</inist>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/EdenteV2/Data/PascalFrancis/Corpus

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000258 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/PascalFrancis/Corpus/biblio.hfd -nk 000258 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Wicri/Santé
   |area=    EdenteV2
   |flux=    PascalFrancis
   |étape=   Corpus
   |type=    RBID
   |clé=     Pascal:09-0450367
   |texte=   Cyclosporine A enhances apoptosis in gingival keratinocytes of rats and in OECM1 cells via the mitochondrial pathway
}}

This area was generated with Dilib version V0.6.32.
Data generation: Thu Nov 30 15:26:48 2017. Site generation: Tue Mar 8 16:36:20 2022

	Serveur d'exploration sur le patient édenté
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration sur le patient édenté

Cyclosporine A enhances apoptosis in gingival keratinocytes of rats and in OECM1 cells via the mitochondrial pathway

Cyclosporine A enhances apoptosis in gingival keratinocytes of rats and in OECM1 cells via the mitochondrial pathway

Source :

Descripteurs français

English descriptors

Abstract

Notice en format standard (ISO 2709)

Format Inist (serveur)

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri