Carbon Monoxide-Releasing Molecule-3 Suppresses Tumor Necrosis Factor-α- and Interleukin-1β-Induced Expression of Junctional Molecules on Human Gingival Fibroblasts via the Heme Oxygenase-1 Pathway
Human gingival fibroblast barrier dysfunction caused by inflammation contributes to gingivitis and can lead to inflammatory periodontal disease. The disease features include upregulated epithelial permeability, increased inflammatory mediators, and downregulated junctional complex molecules. Carbon...
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| Format: | Article |
| Language: | English |
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Wiley
2020-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2020/6302391 |
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| author | Jia Lv Yongsheng Liu Shuhan Jia Yuna Zhang Haoyang Tian Jingyuan Li Hui Song |
| author_facet | Jia Lv Yongsheng Liu Shuhan Jia Yuna Zhang Haoyang Tian Jingyuan Li Hui Song |
| author_sort | Jia Lv |
| collection | DOAJ |
| description | Human gingival fibroblast barrier dysfunction caused by inflammation contributes to gingivitis and can lead to inflammatory periodontal disease. The disease features include upregulated epithelial permeability, increased inflammatory mediators, and downregulated junctional complex molecules. Carbon monoxide- (CO-) releasing molecule-3 (CORM-3) is a water-soluble compound that has demonstrated anti-inflammatory effects in in vitro and in vivo studies. In this study, we aimed to investigate the effects of CORM-3 on the expression of tight and adherens junction molecules on human gingival fibroblasts (HGFs) stimulated with tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). HGFs were cultured from the explants of normal human gingival tissues, which were stimulated in the presence or absence of CORM-3. Epithelial barrier function was evaluated by paracellular permeability and junctional complex molecule expression analyses. The protein and mRNA expression levels of adherens junction molecules (VE-cadherin and β-catenin) and tight junction molecules (zona occludens-1, ZO-1) were studied using western blot analysis and reverse transcription-quantitative polymerase chain reaction (RT-PCR). The mRNA and protein expression levels of these cytokines were also analyzed in HGFs transiently transfected with HO-1 small interfering RNA (siRNA) in response to TNF-α and IL-1β stimulation. CORM-3 reduced permeability and enhanced the expression of junctional complex molecules (ZO-1, VE-cadherin, and β-catenin) in TNF-α- and IL-1β-induced HGFs. However, these effects of CORM-3 were attenuated when HO-1 siRNA was transiently transfected in HGFs. These findings indicate that CORM-3 exerts anti-inflammatory effects on TNF-α- and IL-1β-stimulated HGFs via the HO-1 pathway, which suggests the promising potential of CORM-3 in the treatment of inflammatory periodontal disease. |
| format | Article |
| id | doaj-art-43169b89a3904aafaf3383fe1eb0f014 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2020-01-01 |
| publisher | Wiley |
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| series | Mediators of Inflammation |
| spelling | doaj-art-43169b89a3904aafaf3383fe1eb0f0142025-02-03T01:05:02ZengWileyMediators of Inflammation0962-93511466-18612020-01-01202010.1155/2020/63023916302391Carbon Monoxide-Releasing Molecule-3 Suppresses Tumor Necrosis Factor-α- and Interleukin-1β-Induced Expression of Junctional Molecules on Human Gingival Fibroblasts via the Heme Oxygenase-1 PathwayJia Lv0Yongsheng Liu1Shuhan Jia2Yuna Zhang3Haoyang Tian4Jingyuan Li5Hui Song6Department of VIP Center, School and Hospital of Stomatology, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration, No. 44-1 Wenhua Road West, 250012 Jinan, Shandong, ChinaDepartment of VIP Center, School and Hospital of Stomatology, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration, No. 44-1 Wenhua Road West, 250012 Jinan, Shandong, ChinaDepartment of VIP Center, School and Hospital of Stomatology, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration, No. 44-1 Wenhua Road West, 250012 Jinan, Shandong, ChinaDepartment of VIP Center, School and Hospital of Stomatology, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration, No. 44-1 Wenhua Road West, 250012 Jinan, Shandong, ChinaDepartment of VIP Center, School and Hospital of Stomatology, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration, No. 44-1 Wenhua Road West, 250012 Jinan, Shandong, ChinaDepartment of VIP Center, School and Hospital of Stomatology, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration, No. 44-1 Wenhua Road West, 250012 Jinan, Shandong, ChinaDepartment of VIP Center, School and Hospital of Stomatology, Shandong University & Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration, No. 44-1 Wenhua Road West, 250012 Jinan, Shandong, ChinaHuman gingival fibroblast barrier dysfunction caused by inflammation contributes to gingivitis and can lead to inflammatory periodontal disease. The disease features include upregulated epithelial permeability, increased inflammatory mediators, and downregulated junctional complex molecules. Carbon monoxide- (CO-) releasing molecule-3 (CORM-3) is a water-soluble compound that has demonstrated anti-inflammatory effects in in vitro and in vivo studies. In this study, we aimed to investigate the effects of CORM-3 on the expression of tight and adherens junction molecules on human gingival fibroblasts (HGFs) stimulated with tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). HGFs were cultured from the explants of normal human gingival tissues, which were stimulated in the presence or absence of CORM-3. Epithelial barrier function was evaluated by paracellular permeability and junctional complex molecule expression analyses. The protein and mRNA expression levels of adherens junction molecules (VE-cadherin and β-catenin) and tight junction molecules (zona occludens-1, ZO-1) were studied using western blot analysis and reverse transcription-quantitative polymerase chain reaction (RT-PCR). The mRNA and protein expression levels of these cytokines were also analyzed in HGFs transiently transfected with HO-1 small interfering RNA (siRNA) in response to TNF-α and IL-1β stimulation. CORM-3 reduced permeability and enhanced the expression of junctional complex molecules (ZO-1, VE-cadherin, and β-catenin) in TNF-α- and IL-1β-induced HGFs. However, these effects of CORM-3 were attenuated when HO-1 siRNA was transiently transfected in HGFs. These findings indicate that CORM-3 exerts anti-inflammatory effects on TNF-α- and IL-1β-stimulated HGFs via the HO-1 pathway, which suggests the promising potential of CORM-3 in the treatment of inflammatory periodontal disease.http://dx.doi.org/10.1155/2020/6302391 |
| spellingShingle | Jia Lv Yongsheng Liu Shuhan Jia Yuna Zhang Haoyang Tian Jingyuan Li Hui Song Carbon Monoxide-Releasing Molecule-3 Suppresses Tumor Necrosis Factor-α- and Interleukin-1β-Induced Expression of Junctional Molecules on Human Gingival Fibroblasts via the Heme Oxygenase-1 Pathway Mediators of Inflammation |
| title | Carbon Monoxide-Releasing Molecule-3 Suppresses Tumor Necrosis Factor-α- and Interleukin-1β-Induced Expression of Junctional Molecules on Human Gingival Fibroblasts via the Heme Oxygenase-1 Pathway |
| title_full | Carbon Monoxide-Releasing Molecule-3 Suppresses Tumor Necrosis Factor-α- and Interleukin-1β-Induced Expression of Junctional Molecules on Human Gingival Fibroblasts via the Heme Oxygenase-1 Pathway |
| title_fullStr | Carbon Monoxide-Releasing Molecule-3 Suppresses Tumor Necrosis Factor-α- and Interleukin-1β-Induced Expression of Junctional Molecules on Human Gingival Fibroblasts via the Heme Oxygenase-1 Pathway |
| title_full_unstemmed | Carbon Monoxide-Releasing Molecule-3 Suppresses Tumor Necrosis Factor-α- and Interleukin-1β-Induced Expression of Junctional Molecules on Human Gingival Fibroblasts via the Heme Oxygenase-1 Pathway |
| title_short | Carbon Monoxide-Releasing Molecule-3 Suppresses Tumor Necrosis Factor-α- and Interleukin-1β-Induced Expression of Junctional Molecules on Human Gingival Fibroblasts via the Heme Oxygenase-1 Pathway |
| title_sort | carbon monoxide releasing molecule 3 suppresses tumor necrosis factor α and interleukin 1β induced expression of junctional molecules on human gingival fibroblasts via the heme oxygenase 1 pathway |
| url | http://dx.doi.org/10.1155/2020/6302391 |
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