Modulation of lectin-like oxidized low-density lipoprotein receptor-1 by Porphyromonas gingivalis promoting progression of atherosclerosis in apolipoprotein E-/- mice
Porphyromonas gingivalis (P. gingivalis), the primary pathogenic bacterium in periodontitis, can infiltrate the cardiovascular system via the bloodstream and actively contribute to various pathological processes associated with atherosclerosis. The scavenger receptor lectin-like oxidized low-density...
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Published in | Journal of dental sciences Vol. 20; no. 2; pp. 754 - 763 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
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Netherlands
Elsevier B.V
01.04.2025
Association for Dental Sciences of the Republic of China Elsevier |
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Abstract | Porphyromonas gingivalis (P. gingivalis), the primary pathogenic bacterium in periodontitis, can infiltrate the cardiovascular system via the bloodstream and actively contribute to various pathological processes associated with atherosclerosis. The scavenger receptor lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) plays a crucial role in atherosclerosis pathogenesis. Previous studies have shown that LOX-1 is involved in endothelial cell activation injury, monocyte migration, and adhesion to endothelial cells induced by P. gingivalis. The objective of this study was to further investigate the potential role of LOX-1 in promoting P. gingivalis-induced atherosclerosis in mice.
Using apolipoprotein E (APOE)-/- mice fed with high-fat diet for an established model. Intravenous injection of P. gingivalis was performed to create P. gingivalis blood model while intraperitoneal injection of Polyinosinic-polycytidylic acid (Poly (I:C)) served as an inhibitor for LOX-1. After 12 weeks, plaques and blood lipids were examined.
Results showed that induction with P. gingivalis led to increased expression of LOX-1 in both the aortic root and blood samples, increased plaque area, reduced plaque stability, elevated expression levels of vascular adhesion molecule-1(VCAM-1), Interleukin-6(IL-6) and M1 macrophages. However, pretreatment with Poly (I:C) resulted in decreased plaque area improved plaque stability and reduced expression levels of VCAM-1 and IL-6.
These findings suggest that LOX-1 may serve as an intermediary factor promoting atherosclerosis associated with periodontitis. |
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AbstractList | (
), the primary pathogenic bacterium in periodontitis, can infiltrate the cardiovascular system via the bloodstream and actively contribute to various pathological processes associated with atherosclerosis. The scavenger receptor lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) plays a crucial role in atherosclerosis pathogenesis. Previous studies have shown that LOX-1 is involved in endothelial cell activation injury, monocyte migration, and adhesion to endothelial cells induced by
. The objective of this study was to further investigate the potential role of LOX-1 in promoting
-induced atherosclerosis in mice.
Using apolipoprotein E (APOE)
mice fed with high-fat diet for an established model. Intravenous injection of
was performed to create
blood model while intraperitoneal injection of Polyinosinic-polycytidylic acid (Poly (I:C)) served as an inhibitor for LOX-1. After 12 weeks, plaques and blood lipids were examined.
Results showed that induction with
led to increased expression of LOX-1 in both the aortic root and blood samples, increased plaque area, reduced plaque stability, elevated expression levels of vascular adhesion molecule-1(VCAM-1), Interleukin-6(IL-6) and M1 macrophages. However, pretreatment with Poly (I:C) resulted in decreased plaque area improved plaque stability and reduced expression levels of VCAM-1 and IL-6.
These findings suggest that LOX-1 may serve as an intermediary factor promoting atherosclerosis associated with periodontitis. Background/Purpose: Porphyromonas gingivalis (P. gingivalis), the primary pathogenic bacterium in periodontitis, can infiltrate the cardiovascular system via the bloodstream and actively contribute to various pathological processes associated with atherosclerosis. The scavenger receptor lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) plays a crucial role in atherosclerosis pathogenesis. Previous studies have shown that LOX-1 is involved in endothelial cell activation injury, monocyte migration, and adhesion to endothelial cells induced by P. gingivalis. The objective of this study was to further investigate the potential role of LOX-1 in promoting P. gingivalis-induced atherosclerosis in mice. Materials and methods: Using apolipoprotein E (APOE)-/- mice fed with high-fat diet for an established model. Intravenous injection of P. gingivalis was performed to create P. gingivalis blood model while intraperitoneal injection of Polyinosinic-polycytidylic acid (Poly (I:C)) served as an inhibitor for LOX-1. After 12 weeks, plaques and blood lipids were examined. Results: Results showed that induction with P. gingivalis led to increased expression of LOX-1 in both the aortic root and blood samples, increased plaque area, reduced plaque stability, elevated expression levels of vascular adhesion molecule-1(VCAM-1), Interleukin-6(IL-6) and M1 macrophages. However, pretreatment with Poly (I:C) resulted in decreased plaque area improved plaque stability and reduced expression levels of VCAM-1 and IL-6. Conclusion: These findings suggest that LOX-1 may serve as an intermediary factor promoting atherosclerosis associated with periodontitis. Porphyromonas gingivalis (P. gingivalis), the primary pathogenic bacterium in periodontitis, can infiltrate the cardiovascular system via the bloodstream and actively contribute to various pathological processes associated with atherosclerosis. The scavenger receptor lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) plays a crucial role in atherosclerosis pathogenesis. Previous studies have shown that LOX-1 is involved in endothelial cell activation injury, monocyte migration, and adhesion to endothelial cells induced by P. gingivalis. The objective of this study was to further investigate the potential role of LOX-1 in promoting P. gingivalis-induced atherosclerosis in mice. Using apolipoprotein E (APOE)-/- mice fed with high-fat diet for an established model. Intravenous injection of P. gingivalis was performed to create P. gingivalis blood model while intraperitoneal injection of Polyinosinic-polycytidylic acid (Poly (I:C)) served as an inhibitor for LOX-1. After 12 weeks, plaques and blood lipids were examined. Results showed that induction with P. gingivalis led to increased expression of LOX-1 in both the aortic root and blood samples, increased plaque area, reduced plaque stability, elevated expression levels of vascular adhesion molecule-1(VCAM-1), Interleukin-6(IL-6) and M1 macrophages. However, pretreatment with Poly (I:C) resulted in decreased plaque area improved plaque stability and reduced expression levels of VCAM-1 and IL-6. These findings suggest that LOX-1 may serve as an intermediary factor promoting atherosclerosis associated with periodontitis. AbstractBackground/PurposePorphyromonas gingivalis ( P. gingivalis), the primary pathogenic bacterium in periodontitis, can infiltrate the cardiovascular system via the bloodstream and actively contribute to various pathological processes associated with atherosclerosis. The scavenger receptor lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) plays a crucial role in atherosclerosis pathogenesis. Previous studies have shown that LOX-1 is involved in endothelial cell activation injury, monocyte migration, and adhesion to endothelial cells induced by P. gingivalis. The objective of this study was to further investigate the potential role of LOX-1 in promoting P. gingivalis-induced atherosclerosis in mice. Materials and methodsUsing apolipoprotein E (APOE) -/- mice fed with high-fat diet for an established model. Intravenous injection of P. gingivalis was performed to create P. gingivalis blood model while intraperitoneal injection of Polyinosinic-polycytidylic acid (Poly (I:C)) served as an inhibitor for LOX-1. After 12 weeks, plaques and blood lipids were examined. ResultsResults showed that induction with P. gingivalis led to increased expression of LOX-1 in both the aortic root and blood samples, increased plaque area, reduced plaque stability, elevated expression levels of vascular adhesion molecule-1(VCAM-1), Interleukin-6(IL-6) and M1 macrophages. However, pretreatment with Poly (I:C) resulted in decreased plaque area improved plaque stability and reduced expression levels of VCAM-1 and IL-6. ConclusionThese findings suggest that LOX-1 may serve as an intermediary factor promoting atherosclerosis associated with periodontitis. |
Author | Zhang, Shengnan Liu, Jianru Ouyang, Xiangying Lyu, Peiying Wang, Yuanbo Zhong, Jinsheng |
Author_xml | – sequence: 1 givenname: Shengnan surname: Zhang fullname: Zhang, Shengnan organization: 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, China – sequence: 2 givenname: Jianru surname: Liu fullname: Liu, Jianru organization: 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, China – sequence: 3 givenname: Xiangying orcidid: 0000-0003-3703-0847 surname: Ouyang fullname: Ouyang, Xiangying email: kqouyangxy@bjmu.edu.cn organization: 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, China – sequence: 4 givenname: Peiying surname: Lyu fullname: Lyu, Peiying organization: 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, China – sequence: 5 givenname: Yuanbo surname: Wang fullname: Wang, Yuanbo organization: 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, China – sequence: 6 givenname: Jinsheng surname: Zhong fullname: Zhong, Jinsheng organization: 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, China |
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Keywords | Porphyromonas gingivalis Poly(I:C) LOX-1 Atherosclerosis Plaque Macrophage |
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Snippet | Porphyromonas gingivalis (P. gingivalis), the primary pathogenic bacterium in periodontitis, can infiltrate the cardiovascular system via the bloodstream and... AbstractBackground/PurposePorphyromonas gingivalis ( P. gingivalis), the primary pathogenic bacterium in periodontitis, can infiltrate the cardiovascular... ( ), the primary pathogenic bacterium in periodontitis, can infiltrate the cardiovascular system via the bloodstream and actively contribute to various... Background/Purpose: Porphyromonas gingivalis (P. gingivalis), the primary pathogenic bacterium in periodontitis, can infiltrate the cardiovascular system via... |
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SubjectTerms | Advanced Basic Science Atherosclerosis Dentistry LOX-1 Macrophage Original Plaque Poly(I:C) Porphyromonas gingivalis |
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Title | Modulation of lectin-like oxidized low-density lipoprotein receptor-1 by Porphyromonas gingivalis promoting progression of atherosclerosis in apolipoprotein E-/- mice |
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