Cyclophilin a increases CD68+ cell infiltration in rat experimental periodontitis
Cyclophilin A (CyPA) is a potent chemokine, which can directly induce leukocyte chemotaxis and contribute to the pathogenesis of inflammation-mediated diseases. This study is to observe the expression and distribution of CyPA and CD68 + cells in the histopathogenesis of rat ligation-induced experime...
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| Veröffentlicht in: | Journal of molecular histology 2018-04, Vol.49 (2), p.157-164 |
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| creator | Xue, Lande Su, Linwang Zhao, Li Li, Jianxia Du, Yi Yu, Xijiao |
| description | Cyclophilin A (CyPA) is a potent chemokine, which can directly induce leukocyte chemotaxis and contribute to the pathogenesis of inflammation-mediated diseases. This study is to observe the expression and distribution of CyPA and CD68
+
cells in the histopathogenesis of rat ligation-induced experimental periodontitis, and assess the role of CyPA in CD68
+
cell infiltration in rat experimental periodontitis. Experimental periodontitis was induced by ligation according to our previous method. CyPA expression in gingival tissues was detected by western blotting. Immunohistochemistry was applied for CyPA and CD68 distribution. For further certifying the role of CyPA in CD68
+
cell infiltration, the right mandibular first molar received 0.1 μM CyPA locally by gingival injection every 2 days (L + C group), while the left mandibular first molar received saline as a control group (L group). The number of CD68
+
cells in the experimental periodontitis was observed by immunohistochemistry. Alveolar bone destruction was assessed by micro-computerized tomography (micro-CT). Osteoclast was observed through TRAP staining. Nuclear factor (NF)-κB phospho-p65 (p p65) and phosphor-IκBα (p IκBα) expressions were detected to investigate NF-κB activation. CyPA showed an increasing trend at 1–6 weeks after ligation. CyPA and CD68
+
cells were present in the gingival inflammatory infiltration, and participated in alveolar bone destruction. In the L + C group, the number of CD68
+
cells was increased compared with the L group, and greater alveolar bone destruction was observed. NF-κB p p65 and p IκBα expressions were upregulated in the L + C group compared with the L group indicating NF-κB activation. CyPA increases CD68
+
cell infiltration in rat experimental periodontitis, suggesting CyPA might be an anti-inflammatory therapeutic target. |
| doi_str_mv | 10.1007/s10735-018-9755-6 |
| format | Article |
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+
cells in the histopathogenesis of rat ligation-induced experimental periodontitis, and assess the role of CyPA in CD68
+
cell infiltration in rat experimental periodontitis. Experimental periodontitis was induced by ligation according to our previous method. CyPA expression in gingival tissues was detected by western blotting. Immunohistochemistry was applied for CyPA and CD68 distribution. For further certifying the role of CyPA in CD68
+
cell infiltration, the right mandibular first molar received 0.1 μM CyPA locally by gingival injection every 2 days (L + C group), while the left mandibular first molar received saline as a control group (L group). The number of CD68
+
cells in the experimental periodontitis was observed by immunohistochemistry. Alveolar bone destruction was assessed by micro-computerized tomography (micro-CT). Osteoclast was observed through TRAP staining. Nuclear factor (NF)-κB phospho-p65 (p p65) and phosphor-IκBα (p IκBα) expressions were detected to investigate NF-κB activation. CyPA showed an increasing trend at 1–6 weeks after ligation. CyPA and CD68
+
cells were present in the gingival inflammatory infiltration, and participated in alveolar bone destruction. In the L + C group, the number of CD68
+
cells was increased compared with the L group, and greater alveolar bone destruction was observed. NF-κB p p65 and p IκBα expressions were upregulated in the L + C group compared with the L group indicating NF-κB activation. CyPA increases CD68
+
cell infiltration in rat experimental periodontitis, suggesting CyPA might be an anti-inflammatory therapeutic target.</description><identifier>ISSN: 1567-2379</identifier><identifier>EISSN: 1567-2387</identifier><identifier>DOI: 10.1007/s10735-018-9755-6</identifier><identifier>PMID: 29318411</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Alveolar bone ; Biomedical and Life Sciences ; Biomedicine ; Cell activation ; Cell Biology ; Chemotaxis ; Computed tomography ; Developmental Biology ; Gingiva ; Gum disease ; Immunohistochemistry ; Inflammation ; Life Sciences ; Mandible ; NF-κB protein ; Original Paper ; Periodontitis ; Western blotting</subject><ispartof>Journal of molecular histology, 2018-04, Vol.49 (2), p.157-164</ispartof><rights>Springer Science+Business Media B.V., part of Springer Nature 2018</rights><rights>Journal of Molecular Histology is a copyright of Springer, (2018). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-a2aaefaaf49b2b70c39c63fe33828b838ae2b9dccc8a1854cb79b653998a994a3</citedby><cites>FETCH-LOGICAL-c372t-a2aaefaaf49b2b70c39c63fe33828b838ae2b9dccc8a1854cb79b653998a994a3</cites><orcidid>0000-0002-9289-5520</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10735-018-9755-6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10735-018-9755-6$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29318411$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xue, Lande</creatorcontrib><creatorcontrib>Su, Linwang</creatorcontrib><creatorcontrib>Zhao, Li</creatorcontrib><creatorcontrib>Li, Jianxia</creatorcontrib><creatorcontrib>Du, Yi</creatorcontrib><creatorcontrib>Yu, Xijiao</creatorcontrib><title>Cyclophilin a increases CD68+ cell infiltration in rat experimental periodontitis</title><title>Journal of molecular histology</title><addtitle>J Mol Hist</addtitle><addtitle>J Mol Histol</addtitle><description>Cyclophilin A (CyPA) is a potent chemokine, which can directly induce leukocyte chemotaxis and contribute to the pathogenesis of inflammation-mediated diseases. This study is to observe the expression and distribution of CyPA and CD68
+
cells in the histopathogenesis of rat ligation-induced experimental periodontitis, and assess the role of CyPA in CD68
+
cell infiltration in rat experimental periodontitis. Experimental periodontitis was induced by ligation according to our previous method. CyPA expression in gingival tissues was detected by western blotting. Immunohistochemistry was applied for CyPA and CD68 distribution. For further certifying the role of CyPA in CD68
+
cell infiltration, the right mandibular first molar received 0.1 μM CyPA locally by gingival injection every 2 days (L + C group), while the left mandibular first molar received saline as a control group (L group). The number of CD68
+
cells in the experimental periodontitis was observed by immunohistochemistry. Alveolar bone destruction was assessed by micro-computerized tomography (micro-CT). Osteoclast was observed through TRAP staining. Nuclear factor (NF)-κB phospho-p65 (p p65) and phosphor-IκBα (p IκBα) expressions were detected to investigate NF-κB activation. CyPA showed an increasing trend at 1–6 weeks after ligation. CyPA and CD68
+
cells were present in the gingival inflammatory infiltration, and participated in alveolar bone destruction. In the L + C group, the number of CD68
+
cells was increased compared with the L group, and greater alveolar bone destruction was observed. NF-κB p p65 and p IκBα expressions were upregulated in the L + C group compared with the L group indicating NF-κB activation. CyPA increases CD68
+
cell infiltration in rat experimental periodontitis, suggesting CyPA might be an anti-inflammatory therapeutic target.</description><subject>Alveolar bone</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell activation</subject><subject>Cell Biology</subject><subject>Chemotaxis</subject><subject>Computed tomography</subject><subject>Developmental Biology</subject><subject>Gingiva</subject><subject>Gum disease</subject><subject>Immunohistochemistry</subject><subject>Inflammation</subject><subject>Life Sciences</subject><subject>Mandible</subject><subject>NF-κB protein</subject><subject>Original Paper</subject><subject>Periodontitis</subject><subject>Western blotting</subject><issn>1567-2379</issn><issn>1567-2387</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kF1LwzAUhoMobk5_gDdS8EaQaj7aJudS6icMRNDrkGapZnTNTFpw_96UziGCV3mT85w357wInRJ8RTDm14FgzvIUE5ECz_O02ENTkhc8pUzw_Z3mMEFHISwxpqLI4BBNKDAiMkKm6KXc6MatP2xj20QlttXeqGBCUt4W4jLRpmniY22bzqvOujZekqgS87U23q5M26kmGaRbuLaznQ3H6KBWTTAn23OG3u7vXsvHdP788FTezFPNOO1SRZUytVJ1BhWtONYMdMFqw5igohJMKEMrWGithSIiz3TFoSpyBiAUQKbYDF2MvmvvPnsTOrmyYZhXtcb1QRIQkOdAWRbR8z_o0vW-jdNFCigXnIGIFBkp7V0I3tRyHTdUfiMJlkPecsxbxrzlkLcsYs_Z1rmvVmax6_gJOAJ0BEIste_G__r6X9dvPFqLDQ</recordid><startdate>20180401</startdate><enddate>20180401</enddate><creator>Xue, Lande</creator><creator>Su, Linwang</creator><creator>Zhao, Li</creator><creator>Li, Jianxia</creator><creator>Du, Yi</creator><creator>Yu, Xijiao</creator><general>Springer Netherlands</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-9289-5520</orcidid></search><sort><creationdate>20180401</creationdate><title>Cyclophilin a increases CD68+ cell infiltration in rat experimental periodontitis</title><author>Xue, Lande ; Su, Linwang ; Zhao, Li ; Li, Jianxia ; Du, Yi ; Yu, Xijiao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-a2aaefaaf49b2b70c39c63fe33828b838ae2b9dccc8a1854cb79b653998a994a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Alveolar bone</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell activation</topic><topic>Cell Biology</topic><topic>Chemotaxis</topic><topic>Computed tomography</topic><topic>Developmental Biology</topic><topic>Gingiva</topic><topic>Gum disease</topic><topic>Immunohistochemistry</topic><topic>Inflammation</topic><topic>Life Sciences</topic><topic>Mandible</topic><topic>NF-κB protein</topic><topic>Original Paper</topic><topic>Periodontitis</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xue, Lande</creatorcontrib><creatorcontrib>Su, Linwang</creatorcontrib><creatorcontrib>Zhao, Li</creatorcontrib><creatorcontrib>Li, Jianxia</creatorcontrib><creatorcontrib>Du, Yi</creatorcontrib><creatorcontrib>Yu, Xijiao</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of molecular histology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xue, Lande</au><au>Su, Linwang</au><au>Zhao, Li</au><au>Li, Jianxia</au><au>Du, Yi</au><au>Yu, Xijiao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cyclophilin a increases CD68+ cell infiltration in rat experimental periodontitis</atitle><jtitle>Journal of molecular histology</jtitle><stitle>J Mol Hist</stitle><addtitle>J Mol Histol</addtitle><date>2018-04-01</date><risdate>2018</risdate><volume>49</volume><issue>2</issue><spage>157</spage><epage>164</epage><pages>157-164</pages><issn>1567-2379</issn><eissn>1567-2387</eissn><abstract>Cyclophilin A (CyPA) is a potent chemokine, which can directly induce leukocyte chemotaxis and contribute to the pathogenesis of inflammation-mediated diseases. This study is to observe the expression and distribution of CyPA and CD68
+
cells in the histopathogenesis of rat ligation-induced experimental periodontitis, and assess the role of CyPA in CD68
+
cell infiltration in rat experimental periodontitis. Experimental periodontitis was induced by ligation according to our previous method. CyPA expression in gingival tissues was detected by western blotting. Immunohistochemistry was applied for CyPA and CD68 distribution. For further certifying the role of CyPA in CD68
+
cell infiltration, the right mandibular first molar received 0.1 μM CyPA locally by gingival injection every 2 days (L + C group), while the left mandibular first molar received saline as a control group (L group). The number of CD68
+
cells in the experimental periodontitis was observed by immunohistochemistry. Alveolar bone destruction was assessed by micro-computerized tomography (micro-CT). Osteoclast was observed through TRAP staining. Nuclear factor (NF)-κB phospho-p65 (p p65) and phosphor-IκBα (p IκBα) expressions were detected to investigate NF-κB activation. CyPA showed an increasing trend at 1–6 weeks after ligation. CyPA and CD68
+
cells were present in the gingival inflammatory infiltration, and participated in alveolar bone destruction. In the L + C group, the number of CD68
+
cells was increased compared with the L group, and greater alveolar bone destruction was observed. NF-κB p p65 and p IκBα expressions were upregulated in the L + C group compared with the L group indicating NF-κB activation. CyPA increases CD68
+
cell infiltration in rat experimental periodontitis, suggesting CyPA might be an anti-inflammatory therapeutic target.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>29318411</pmid><doi>10.1007/s10735-018-9755-6</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-9289-5520</orcidid></addata></record> |
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| subjects | Alveolar bone Biomedical and Life Sciences Biomedicine Cell activation Cell Biology Chemotaxis Computed tomography Developmental Biology Gingiva Gum disease Immunohistochemistry Inflammation Life Sciences Mandible NF-κB protein Original Paper Periodontitis Western blotting |
| title | Cyclophilin a increases CD68+ cell infiltration in rat experimental periodontitis |
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