The role of Interleukin-7 in Porphyromonas gingivalis-stimulated vascular calcification
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Periodontal disease has been implicated in the progression of various systemic diseases, including chronic kidneydisease (CKD). Recent evidence suggests that infection of Porphyromonas gingivalis, a major periodontal pathogen,may also contribute to vascular calcification in patients with CKD. In the present study, antibody array analysisof serum samples from CKD mice administered with oral P. gingivalis revealed significant alterations in proteinexpression profiles, with notable interleukin-7 (IL-7) upregulation. We demonstrated that P. gingivalis infectionenhances the inorganic phosphate-induced calcification of vascular smooth muscle cells (VSMCs), a pathologicalprocess that is characteristically accelerated in CKD. Notably, IL-7 expression was significantly upregulated inthe P. gingivalis-stimulated calcification of VSMCs. Moreover, IL-7 knockdown in VSMCs markedly attenuated theP. gingivalis-stimulated calcification of VSMCs and suppressed the expression of osteogenic markers, includingalkaline phosphatase and Runt-related transcription factor 2. These findings suggest that IL-7 plays a crucial role inP. gingivalis-stimulated vascular calcification, potentially providing new therapeutic targets for preventing vascularcalcification in CKD patients with periodontal infection.
Abstract
Periodontal disease has been implicated in the progression of various systemic diseases, including chronic kidneydisease (CKD). Recent evidence suggests that infection of Porphyromonas gingivalis, a major periodontal pathogen,may also contribute to vascular calcification in patients with CKD. In the present study, antibody array analysisof serum samples from CKD mice administered with oral P. gingivalis revealed significant alterations in proteinexpression profiles, with notable interleukin-7 (IL-7) upregulation. We demonstrated that P. gingivalis infectionenhances the inorganic phosphate-induced calcification of vascular smooth muscle cells (VSMCs), a pathologicalprocess that is characteristically accelerated in CKD. Notably, IL-7 expression was significantly upregulated inthe P. gingivalis-stimulated calcification of VSMCs. Moreover, IL-7 knockdown in VSMCs markedly attenuated theP. gingivalis-stimulated calcification of VSMCs and suppressed the expression of osteogenic markers, includingalkaline phosphatase and Runt-related transcription factor 2. These findings suggest that IL-7 plays a crucial role inP. gingivalis-stimulated vascular calcification, potentially providing new therapeutic targets for preventing vascularcalcification in CKD patients with periodontal infection.
참고문헌 (28)
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