Polyinosinic-polycytidylic acid modulates Porphyromonas gingivalis-induced cell apoptosis via the janus kinase/ signal transducer and activator of transcription signaling pathway
Background/Purpose: Porphyromonas gingivalis (P. gingivalis) has been shown to induce apoptosis in endothelial cells and contribute to the progression of atherosclerosis. While Polyinosinic-polycytidylic acid (Poly (I:C)) is known to activate the innate immune response against infections, its potent...
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Elsevier
2025-04-01
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| Series: | Journal of Dental Sciences |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S1991790224003325 |
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| author | Shengnan Zhang Jianru Liu Xiangying Ouyang Wenyi Liu Yuanbo Wang Jinsheng Zhong |
| author_facet | Shengnan Zhang Jianru Liu Xiangying Ouyang Wenyi Liu Yuanbo Wang Jinsheng Zhong |
| author_sort | Shengnan Zhang |
| collection | DOAJ |
| description | Background/Purpose: Porphyromonas gingivalis (P. gingivalis) has been shown to induce apoptosis in endothelial cells and contribute to the progression of atherosclerosis. While Polyinosinic-polycytidylic acid (Poly (I:C)) is known to activate the innate immune response against infections, its potential interference with P. gingivalis-induced atherosclerosis remains unclear. This study aimed to elucidate the role and underlying mechanisms of Poly (I:C) in mediating human umbilical vein endothelial cells (HUVECs) apoptosis induced by P. gingivalis. Materials and methods: A mice model of atherosclerosis and a model of P. gingivalis-induced bacteremia were established to investigate the effects of Poly (I:C) on P. gingivalis-induced apoptosis in the aortic root, as well as the expression levels of apoptosis-related proteins including Caspase 3, Caspase 9, Bax, and Bcl-2. Subsequently, HUVECs were cultured in vitro to compare cell apoptosis and the expression of these apoptosis-related proteins under stimulation with P. gingivalis, both with and without Poly (I:C) treatment; additionally, the activation status of the JAK/STAT signaling pathway was assessed. Results: The administration of Poly (I:C) diminished apoptosis in the aortic root cells of mice, enhanced the expression of the anti-apoptotic protein Bcl-2, and decreased the levels of Bax, Caspase 3 and 9. Furthermore, Poly (I:C) exhibited similar effects on HUVECs cultured in vitro. Additionally, treatment with Poly (I:C) activated the JAK/STAT signaling pathway, while STAT inhibitor was found to attenuate its effects. Conclusion: Poly (I:C) attenuated P. gingivalis-induced cellular apoptosis, with the involvement of the JAK/STAT signaling pathway in this mechanism. |
| format | Article |
| id | doaj-art-ce977d8289f540de985d1cd6edd97553 |
| institution | Kabale University |
| issn | 1991-7902 |
| language | English |
| publishDate | 2025-04-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Journal of Dental Sciences |
| spelling | doaj-art-ce977d8289f540de985d1cd6edd975532025-08-20T03:44:28ZengElsevierJournal of Dental Sciences1991-79022025-04-0120281181810.1016/j.jds.2024.09.021Polyinosinic-polycytidylic acid modulates Porphyromonas gingivalis-induced cell apoptosis via the janus kinase/ signal transducer and activator of transcription signaling pathwayShengnan Zhang0Jianru Liu1Xiangying Ouyang2Wenyi Liu3Yuanbo Wang4Jinsheng Zhong5Department of Periodontology, Peking University School and Hospital of Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Beijing, China; Second Clinical Division, Peking University School and Hospital of Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Beijing, ChinaDepartment of Periodontology, Peking University School and Hospital of Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Beijing, ChinaDepartment of Periodontology, Peking University School and Hospital of Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Beijing, China; Corresponding author. Department of Periodontology, Peking University School and Hospital of Stomatology, No. 22 Zhongguancun South Avenue, Haidian District, Beijing, 100081, China.Department of Periodontology, Peking University School and Hospital of Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Beijing, ChinaDepartment of Periodontology, Peking University School and Hospital of Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Beijing, ChinaDepartment of Periodontology, Peking University School and Hospital of Stomatology & National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Beijing, ChinaBackground/Purpose: Porphyromonas gingivalis (P. gingivalis) has been shown to induce apoptosis in endothelial cells and contribute to the progression of atherosclerosis. While Polyinosinic-polycytidylic acid (Poly (I:C)) is known to activate the innate immune response against infections, its potential interference with P. gingivalis-induced atherosclerosis remains unclear. This study aimed to elucidate the role and underlying mechanisms of Poly (I:C) in mediating human umbilical vein endothelial cells (HUVECs) apoptosis induced by P. gingivalis. Materials and methods: A mice model of atherosclerosis and a model of P. gingivalis-induced bacteremia were established to investigate the effects of Poly (I:C) on P. gingivalis-induced apoptosis in the aortic root, as well as the expression levels of apoptosis-related proteins including Caspase 3, Caspase 9, Bax, and Bcl-2. Subsequently, HUVECs were cultured in vitro to compare cell apoptosis and the expression of these apoptosis-related proteins under stimulation with P. gingivalis, both with and without Poly (I:C) treatment; additionally, the activation status of the JAK/STAT signaling pathway was assessed. Results: The administration of Poly (I:C) diminished apoptosis in the aortic root cells of mice, enhanced the expression of the anti-apoptotic protein Bcl-2, and decreased the levels of Bax, Caspase 3 and 9. Furthermore, Poly (I:C) exhibited similar effects on HUVECs cultured in vitro. Additionally, treatment with Poly (I:C) activated the JAK/STAT signaling pathway, while STAT inhibitor was found to attenuate its effects. Conclusion: Poly (I:C) attenuated P. gingivalis-induced cellular apoptosis, with the involvement of the JAK/STAT signaling pathway in this mechanism.http://www.sciencedirect.com/science/article/pii/S1991790224003325Porphyromonas gingivalisAtherosclerosisPoly(I:C)ApoptosisHuman umbilical vein endothelial cells |
| spellingShingle | Shengnan Zhang Jianru Liu Xiangying Ouyang Wenyi Liu Yuanbo Wang Jinsheng Zhong Polyinosinic-polycytidylic acid modulates Porphyromonas gingivalis-induced cell apoptosis via the janus kinase/ signal transducer and activator of transcription signaling pathway Journal of Dental Sciences Porphyromonas gingivalis Atherosclerosis Poly(I:C) Apoptosis Human umbilical vein endothelial cells |
| title | Polyinosinic-polycytidylic acid modulates Porphyromonas gingivalis-induced cell apoptosis via the janus kinase/ signal transducer and activator of transcription signaling pathway |
| title_full | Polyinosinic-polycytidylic acid modulates Porphyromonas gingivalis-induced cell apoptosis via the janus kinase/ signal transducer and activator of transcription signaling pathway |
| title_fullStr | Polyinosinic-polycytidylic acid modulates Porphyromonas gingivalis-induced cell apoptosis via the janus kinase/ signal transducer and activator of transcription signaling pathway |
| title_full_unstemmed | Polyinosinic-polycytidylic acid modulates Porphyromonas gingivalis-induced cell apoptosis via the janus kinase/ signal transducer and activator of transcription signaling pathway |
| title_short | Polyinosinic-polycytidylic acid modulates Porphyromonas gingivalis-induced cell apoptosis via the janus kinase/ signal transducer and activator of transcription signaling pathway |
| title_sort | polyinosinic polycytidylic acid modulates porphyromonas gingivalis induced cell apoptosis via the janus kinase signal transducer and activator of transcription signaling pathway |
| topic | Porphyromonas gingivalis Atherosclerosis Poly(I:C) Apoptosis Human umbilical vein endothelial cells |
| url | http://www.sciencedirect.com/science/article/pii/S1991790224003325 |
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