Up-regulation of retino-blastoma protein phosphorylation in gingiva after cyclosporine A treatment: an in vivo and in vitro study
Identifieur interne : 000155 ( PascalFrancis/Corpus ); précédent : 000154; suivant : 000156Up-regulation of retino-blastoma protein phosphorylation in gingiva after cyclosporine A treatment: an in vivo and in vitro study
Auteurs : C.-Y. Chiang ; H.-P. Tu ; Y.-T. Chen ; Y.-T. Chin ; T.-M. Lai ; H.-C. Chiu ; S. Nieh ; E. FuSource :
- Journal of periodontal research [ 0022-3484 ] ; 2011.
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- Pascal (Inist)
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Abstract
Background and Objective: Cyclosporine A can induce gingival cell proliferation; however, the precise molecular regulation of the proliferation is uncertain. Therefore, this study was carried out to examine, in vivo and in vitro, the expression of genes and proteins associated with gingival cell proliferation after treatment with cyclosporine A. Material and Methods: Forty Sprague Dawley rats with right maxillary posterior edentulous gingivae were assigned to a cyclosporine A group (30 mg/kg daily of cyclosporine A, administered orally) or a control group (administered mineral oil only). The animals were killed 4 wk after treatment. The edentulous gingivae were dissected out and analyzed for the expression of proliferating cell nuclear antigen (PCNA), cyclin D1, cyclin-dependent kinase 4 (CDK4) and retinoblastoma protein (Rb1) mRNA and/or protein, and phosphorylated Rb1 (pRbl), by real-time RT-PCR or immunohistochemistry. In human gingival fibroblast (HGF) cultures, the expression of PCNA, CDK4, cyclin D1 and Rb1 proteins and Rbl phosphorylation were determined by western blotting after cyclosporine A treatment (0-104 ng/mL). Results: Proliferating cell nuclear antigen and cyclin D1 mRNAs (Pcna and Ccnd1, respectively) were expressed more strongly in the gingivae of cyclosporine A-treated animals than in the gingivae of the controls. Immunohistochemical analyses showed that a greater number of gingival cells stained positive for cyclin D1, CDK4 and pRb1 in the cyclosporine A group than in the control group. Increased expression of cyclin D1, CDK4 and PCNA proteins was observed in HGFs after cyclosporine A treatment. The phosphorylation of Rb1 was enhanced in HGFs after treatment with cyclosporine A at concentrations of 102-103 ng/mL. Conclusion: The increases in cyclin D1, PCNA and CDK4, together with the enhanced phosphorylation of Rb1, suggest that cyclosporine A promotes cell-cycle progression through the G1/S transition in the gingiva.
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| NO : | PASCAL 11-0134974 INIST |
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| ET : | Up-regulation of retino-blastoma protein phosphorylation in gingiva after cyclosporine A treatment: an in vivo and in vitro study |
| AU : | CHIANG (C.-Y.); TU (H.-P.); CHEN (Y.-T.); CHIN (Y.-T.); LAI (T.-M.); CHIU (H.-C.); NIEH (S.); FU (E.) |
| AF : | Department of Periodontology, School of Dentistry, National Defense Medical Center and Tri-Service General Hospital/Taipei/Taïwan (1 aut., 3 aut., 4 aut., 6 aut., 8 aut.); Department of Dental Hygiene, China Medical University/Taichung/Taïwan (2 aut.); Graduate Institute of Life Sciences, National Defense Medical Center/Taipei/Taïwan (4 aut.); Dental Department, Cardinal Tien Hospital/Taipei/Taïwan (5 aut.); Department of Pathology, National Defense Medical Center and Tri-Service General Hospital/Taipei/Taïwan (7 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | Journal of periodontal research; ISSN 0022-3484; Royaume-Uni; Da. 2011; Vol. 46; No. 2; Pp. 158-163; Bibl. 28 ref. |
| LA : | Anglais |
| EA : | Background and Objective: Cyclosporine A can induce gingival cell proliferation; however, the precise molecular regulation of the proliferation is uncertain. Therefore, this study was carried out to examine, in vivo and in vitro, the expression of genes and proteins associated with gingival cell proliferation after treatment with cyclosporine A. Material and Methods: Forty Sprague Dawley rats with right maxillary posterior edentulous gingivae were assigned to a cyclosporine A group (30 mg/kg daily of cyclosporine A, administered orally) or a control group (administered mineral oil only). The animals were killed 4 wk after treatment. The edentulous gingivae were dissected out and analyzed for the expression of proliferating cell nuclear antigen (PCNA), cyclin D1, cyclin-dependent kinase 4 (CDK4) and retinoblastoma protein (Rb1) mRNA and/or protein, and phosphorylated Rb1 (pRbl), by real-time RT-PCR or immunohistochemistry. In human gingival fibroblast (HGF) cultures, the expression of PCNA, CDK4, cyclin D1 and Rb1 proteins and Rbl phosphorylation were determined by western blotting after cyclosporine A treatment (0-104 ng/mL). Results: Proliferating cell nuclear antigen and cyclin D1 mRNAs (Pcna and Ccnd1, respectively) were expressed more strongly in the gingivae of cyclosporine A-treated animals than in the gingivae of the controls. Immunohistochemical analyses showed that a greater number of gingival cells stained positive for cyclin D1, CDK4 and pRb1 in the cyclosporine A group than in the control group. Increased expression of cyclin D1, CDK4 and PCNA proteins was observed in HGFs after cyclosporine A treatment. The phosphorylation of Rb1 was enhanced in HGFs after treatment with cyclosporine A at concentrations of 102-103 ng/mL. Conclusion: The increases in cyclin D1, PCNA and CDK4, together with the enhanced phosphorylation of Rb1, suggest that cyclosporine A promotes cell-cycle progression through the G1/S transition in the gingiva. |
| CC : | 002B10 |
| FD : | Ciclosporine; Traitement; Régulation; Blastome; Protéine rétinoblastome; Phosphorylation; Gencive; In vitro; In vivo; Stomatologie; Immunodépresseur |
| FG : | Inhibiteur de la calcineurine |
| ED : | Ciclosporin; Treatment; Regulation(control); Blastoma; Retinoblastoma protein; Phosphorylation; Gingiva; In vitro; In vivo; Stomatology; Immunosuppressive agent |
| EG : | Calcineurin inhibitor |
| SD : | Ciclosporina; Tratamiento; Regulación; Blastoma; Proteína retinoblastoma; Fosforilación; Encía; In vitro; In vivo; Estomatología; Inmunodepresor |
| LO : | INIST-15072.354000190710500020 |
| ID : | 11-0134974 |
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Tu</name><affiliation><inist:fA14 i1="02"><s1>Department of Dental Hygiene, China Medical University</s1><s2>Taichung</s2><s3>TWN</s3><sZ>2 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>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 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>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>Graduate Institute of Life Sciences, National Defense Medical Center</s1><s2>Taipei</s2><s3>TWN</s3><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Lai, T M" sort="Lai, T M" uniqKey="Lai T" first="T.-M." last="Lai">T.-M. Lai</name><affiliation><inist:fA14 i1="04"><s1>Dental Department, Cardinal Tien Hospital</s1><s2>Taipei</s2><s3>TWN</s3><sZ>5 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>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Nieh, S" sort="Nieh, S" uniqKey="Nieh S" first="S." last="Nieh">S. Nieh</name><affiliation><inist:fA14 i1="05"><s1>Department of Pathology, National Defense Medical Center and Tri-Service General Hospital</s1><s2>Taipei</s2><s3>TWN</s3><sZ>7 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>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">11-0134974</idno><date when="2011">2011</date><idno type="stanalyst">PASCAL 11-0134974 INIST</idno><idno type="RBID">Pascal:11-0134974</idno><idno type="wicri:Area/PascalFrancis/Corpus">000155</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Up-regulation of retino-blastoma protein phosphorylation in gingiva after cyclosporine A treatment: an in vivo and in vitro study</title><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>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation></author><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="02"><s1>Department of Dental Hygiene, China Medical University</s1><s2>Taichung</s2><s3>TWN</s3><sZ>2 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>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 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>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>Graduate Institute of Life Sciences, National Defense Medical Center</s1><s2>Taipei</s2><s3>TWN</s3><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Lai, T M" sort="Lai, T M" uniqKey="Lai T" first="T.-M." last="Lai">T.-M. Lai</name><affiliation><inist:fA14 i1="04"><s1>Dental Department, Cardinal Tien Hospital</s1><s2>Taipei</s2><s3>TWN</s3><sZ>5 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>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Nieh, S" sort="Nieh, S" uniqKey="Nieh S" first="S." last="Nieh">S. Nieh</name><affiliation><inist:fA14 i1="05"><s1>Department of Pathology, National Defense Medical Center and Tri-Service General Hospital</s1><s2>Taipei</s2><s3>TWN</s3><sZ>7 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>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 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="2011">2011</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>Blastoma</term><term>Ciclosporin</term><term>Gingiva</term><term>Immunosuppressive agent</term><term>In vitro</term><term>In vivo</term><term>Phosphorylation</term><term>Regulation(control)</term><term>Retinoblastoma protein</term><term>Stomatology</term><term>Treatment</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Ciclosporine</term><term>Traitement</term><term>Régulation</term><term>Blastome</term><term>Protéine rétinoblastome</term><term>Phosphorylation</term><term>Gencive</term><term>In vitro</term><term>In vivo</term><term>Stomatologie</term><term>Immunodépresseur</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Background and Objective: Cyclosporine A can induce gingival cell proliferation; however, the precise molecular regulation of the proliferation is uncertain. Therefore, this study was carried out to examine, in vivo and in vitro, the expression of genes and proteins associated with gingival cell proliferation after treatment with cyclosporine A. Material and Methods: Forty Sprague Dawley rats with right maxillary posterior edentulous gingivae were assigned to a cyclosporine A group (30 mg/kg daily of cyclosporine A, administered orally) or a control group (administered mineral oil only). The animals were killed 4 wk after treatment. The edentulous gingivae were dissected out and analyzed for the expression of proliferating cell nuclear antigen (PCNA), cyclin D1, cyclin-dependent kinase 4 (CDK4) and retinoblastoma protein (Rb1) mRNA and/or protein, and phosphorylated Rb1 (pRbl), by real-time RT-PCR or immunohistochemistry. In human gingival fibroblast (HGF) cultures, the expression of PCNA, CDK4, cyclin D1 and Rb1 proteins and Rbl phosphorylation were determined by western blotting after cyclosporine A treatment (0-10<sup>4</sup> ng/mL). Results: Proliferating cell nuclear antigen and cyclin D1 mRNAs (Pcna and Ccnd1, respectively) were expressed more strongly in the gingivae of cyclosporine A-treated animals than in the gingivae of the controls. Immunohistochemical analyses showed that a greater number of gingival cells stained positive for cyclin D1, CDK4 and pRb1 in the cyclosporine A group than in the control group. Increased expression of cyclin D1, CDK4 and PCNA proteins was observed in HGFs after cyclosporine A treatment. The phosphorylation of Rb1 was enhanced in HGFs after treatment with cyclosporine A at concentrations of 10<sup>2</sup>-10<sup>3</sup> ng/mL. Conclusion: The increases in cyclin D1, PCNA and CDK4, together with the enhanced phosphorylation of Rb1, suggest that cyclosporine A promotes cell-cycle progression through the G<sub>1</sub>/S transition in the gingiva.</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>46</s2></fA05><fA06><s2>2</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Up-regulation of retino-blastoma protein phosphorylation in gingiva after cyclosporine A treatment: an in vivo and in vitro study</s1></fA08><fA11 i1="01" i2="1"><s1>CHIANG (C.-Y.)</s1></fA11><fA11 i1="02" i2="1"><s1>TU (H.-P.)</s1></fA11><fA11 i1="03" i2="1"><s1>CHEN (Y.-T.)</s1></fA11><fA11 i1="04" i2="1"><s1>CHIN (Y.-T.)</s1></fA11><fA11 i1="05" i2="1"><s1>LAI (T.-M.)</s1></fA11><fA11 i1="06" i2="1"><s1>CHIU (H.-C.)</s1></fA11><fA11 i1="07" i2="1"><s1>NIEH (S.)</s1></fA11><fA11 i1="08" i2="1"><s1>FU (E.)</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>3 aut.</sZ><sZ>4 aut.</sZ><sZ>6 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>2 aut.</sZ></fA14><fA14 i1="03"><s1>Graduate Institute of Life Sciences, National Defense Medical Center</s1><s2>Taipei</s2><s3>TWN</s3><sZ>4 aut.</sZ></fA14><fA14 i1="04"><s1>Dental Department, Cardinal Tien Hospital</s1><s2>Taipei</s2><s3>TWN</s3><sZ>5 aut.</sZ></fA14><fA14 i1="05"><s1>Department of Pathology, National Defense Medical Center and Tri-Service General Hospital</s1><s2>Taipei</s2><s3>TWN</s3><sZ>7 aut.</sZ></fA14><fA20><s1>158-163</s1></fA20><fA21><s1>2011</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>15072</s2><s5>354000190710500020</s5></fA43><fA44><s0>0000</s0><s1>© 2011 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>28 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>11-0134974</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: Cyclosporine A can induce gingival cell proliferation; however, the precise molecular regulation of the proliferation is uncertain. Therefore, this study was carried out to examine, in vivo and in vitro, the expression of genes and proteins associated with gingival cell proliferation after treatment with cyclosporine A. Material and Methods: Forty Sprague Dawley rats with right maxillary posterior edentulous gingivae were assigned to a cyclosporine A group (30 mg/kg daily of cyclosporine A, administered orally) or a control group (administered mineral oil only). The animals were killed 4 wk after treatment. The edentulous gingivae were dissected out and analyzed for the expression of proliferating cell nuclear antigen (PCNA), cyclin D1, cyclin-dependent kinase 4 (CDK4) and retinoblastoma protein (Rb1) mRNA and/or protein, and phosphorylated Rb1 (pRbl), by real-time RT-PCR or immunohistochemistry. In human gingival fibroblast (HGF) cultures, the expression of PCNA, CDK4, cyclin D1 and Rb1 proteins and Rbl phosphorylation were determined by western blotting after cyclosporine A treatment (0-10<sup>4</sup> ng/mL). Results: Proliferating cell nuclear antigen and cyclin D1 mRNAs (Pcna and Ccnd1, respectively) were expressed more strongly in the gingivae of cyclosporine A-treated animals than in the gingivae of the controls. Immunohistochemical analyses showed that a greater number of gingival cells stained positive for cyclin D1, CDK4 and pRb1 in the cyclosporine A group than in the control group. Increased expression of cyclin D1, CDK4 and PCNA proteins was observed in HGFs after cyclosporine A treatment. The phosphorylation of Rb1 was enhanced in HGFs after treatment with cyclosporine A at concentrations of 10<sup>2</sup>-10<sup>3</sup> ng/mL. Conclusion: The increases in cyclin D1, PCNA and CDK4, together with the enhanced phosphorylation of Rb1, suggest that cyclosporine A promotes cell-cycle progression through the G<sub>1</sub>/S transition in the gingiva.</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>Traitement</s0><s5>05</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Treatment</s0><s5>05</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Tratamiento</s0><s5>05</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Régulation</s0><s5>07</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Regulation(control)</s0><s5>07</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Regulación</s0><s5>07</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Blastome</s0><s5>08</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Blastoma</s0><s5>08</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Blastoma</s0><s5>08</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Protéine rétinoblastome</s0><s5>09</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Retinoblastoma protein</s0><s5>09</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Proteína retinoblastoma</s0><s5>09</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Phosphorylation</s0><s5>13</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Phosphorylation</s0><s5>13</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Fosforilación</s0><s5>13</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Gencive</s0><s5>14</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Gingiva</s0><s5>14</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Encía</s0><s5>14</s5></fC03><fC03 i1="08" i2="X" l="FRE"><s0>In vitro</s0><s5>15</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>In vitro</s0><s5>15</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>In vitro</s0><s5>15</s5></fC03><fC03 i1="09" i2="X" l="FRE"><s0>In vivo</s0><s5>16</s5></fC03><fC03 i1="09" i2="X" l="ENG"><s0>In vivo</s0><s5>16</s5></fC03><fC03 i1="09" i2="X" l="SPA"><s0>In vivo</s0><s5>16</s5></fC03><fC03 i1="10" i2="X" l="FRE"><s0>Stomatologie</s0><s5>17</s5></fC03><fC03 i1="10" i2="X" l="ENG"><s0>Stomatology</s0><s5>17</s5></fC03><fC03 i1="10" i2="X" l="SPA"><s0>Estomatología</s0><s5>17</s5></fC03><fC03 i1="11" i2="X" l="FRE"><s0>Immunodépresseur</s0><s5>30</s5></fC03><fC03 i1="11" i2="X" l="ENG"><s0>Immunosuppressive agent</s0><s5>30</s5></fC03><fC03 i1="11" i2="X" l="SPA"><s0>Inmunodepresor</s0><s5>30</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Inhibiteur de la calcineurine</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Calcineurin inhibitor</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Inhibidor calcineurina</s0><s5>37</s5></fC07><fN21><s1>087</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard><server><NO>PASCAL 11-0134974 INIST</NO><ET>Up-regulation of retino-blastoma protein phosphorylation in gingiva after cyclosporine A treatment: an in vivo and in vitro study</ET><AU>CHIANG (C.-Y.); TU (H.-P.); CHEN (Y.-T.); CHIN (Y.-T.); LAI (T.-M.); CHIU (H.-C.); NIEH (S.); FU (E.)</AU><AF>Department of Periodontology, School of Dentistry, National Defense Medical Center and Tri-Service General Hospital/Taipei/Taïwan (1 aut., 3 aut., 4 aut., 6 aut., 8 aut.); Department of Dental Hygiene, China Medical University/Taichung/Taïwan (2 aut.); Graduate Institute of Life Sciences, National Defense Medical Center/Taipei/Taïwan (4 aut.); Dental Department, Cardinal Tien Hospital/Taipei/Taïwan (5 aut.); Department of Pathology, National Defense Medical Center and Tri-Service General Hospital/Taipei/Taïwan (7 aut.)</AF><DT>Publication en série; Niveau analytique</DT><SO>Journal of periodontal research; ISSN 0022-3484; Royaume-Uni; Da. 2011; Vol. 46; No. 2; Pp. 158-163; Bibl. 28 ref.</SO><LA>Anglais</LA><EA>Background and Objective: Cyclosporine A can induce gingival cell proliferation; however, the precise molecular regulation of the proliferation is uncertain. Therefore, this study was carried out to examine, in vivo and in vitro, the expression of genes and proteins associated with gingival cell proliferation after treatment with cyclosporine A. Material and Methods: Forty Sprague Dawley rats with right maxillary posterior edentulous gingivae were assigned to a cyclosporine A group (30 mg/kg daily of cyclosporine A, administered orally) or a control group (administered mineral oil only). The animals were killed 4 wk after treatment. The edentulous gingivae were dissected out and analyzed for the expression of proliferating cell nuclear antigen (PCNA), cyclin D1, cyclin-dependent kinase 4 (CDK4) and retinoblastoma protein (Rb1) mRNA and/or protein, and phosphorylated Rb1 (pRbl), by real-time RT-PCR or immunohistochemistry. In human gingival fibroblast (HGF) cultures, the expression of PCNA, CDK4, cyclin D1 and Rb1 proteins and Rbl phosphorylation were determined by western blotting after cyclosporine A treatment (0-10<sup>4</sup> ng/mL). Results: Proliferating cell nuclear antigen and cyclin D1 mRNAs (Pcna and Ccnd1, respectively) were expressed more strongly in the gingivae of cyclosporine A-treated animals than in the gingivae of the controls. Immunohistochemical analyses showed that a greater number of gingival cells stained positive for cyclin D1, CDK4 and pRb1 in the cyclosporine A group than in the control group. Increased expression of cyclin D1, CDK4 and PCNA proteins was observed in HGFs after cyclosporine A treatment. The phosphorylation of Rb1 was enhanced in HGFs after treatment with cyclosporine A at concentrations of 10<sup>2</sup>-10<sup>3</sup> ng/mL. Conclusion: The increases in cyclin D1, PCNA and CDK4, together with the enhanced phosphorylation of Rb1, suggest that cyclosporine A promotes cell-cycle progression through the G<sub>1</sub>/S transition in the gingiva.</EA><CC>002B10</CC><FD>Ciclosporine; Traitement; Régulation; Blastome; Protéine rétinoblastome; Phosphorylation; Gencive; In vitro; In vivo; Stomatologie; Immunodépresseur</FD><FG>Inhibiteur de la calcineurine</FG><ED>Ciclosporin; Treatment; Regulation(control); Blastoma; Retinoblastoma protein; Phosphorylation; Gingiva; In vitro; In vivo; Stomatology; Immunosuppressive agent</ED><EG>Calcineurin inhibitor</EG><SD>Ciclosporina; Tratamiento; Regulación; Blastoma; Proteína retinoblastoma; Fosforilación; Encía; In vitro; In vivo; Estomatología; Inmunodepresor</SD><LO>INIST-15072.354000190710500020</LO><ID>11-0134974</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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