<i>Porphyromonas gingivalis</i> Lipopolysaccharide Stimulation of Vascular Smooth Muscle Cells Activates Proliferation and Calcification

Liu, Guirong; Deng, Jing; Zhang, Qiang; Song, Wan; Chen, Shulan; Lou, Xiu-Xiu; Zhang, Pengmei; Pan, Keqing

doi:10.1902/jop.2016.150602

Cited by 20 publications

(21 citation statements)

References 48 publications

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“…Recently, further study that investigates the relationship between periodontitis and cardiovascular diseases has focused on the effect of P. gingivalis infection on the pathophysiology of VSMCs. The evidence from these in vitro and in vivo studies showed that the P. gingivalis infection of VSMCs and the stimulation of VSMCs with P. gingivalis ‐derived components regulate the pro‐thrombotic response, proliferation, and calcification of VSMCs (Hokamura et al, ; Liu et al, ; Olsen & Progulske‐Fox, ; Reyes et al, ; Yang et al, ). Moreover, those P. gingivalis ‐derived components include the fimbriae, capsule, and outer vesicles of P. gingivalis and P. gingivalis ‐secreted LPS, haemagglutinins, and proteases (gingipains) (Liu et al, ; Yang et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…SMC calcification, a form of mineralization, was determined by using the Alizarin Red S (ARS) stain, which was used to detect the calcium deposition (Liu et al, ; Yang et al, ). HGPg‐infected HASMCs were fixed with 10% formaldehyde and then stained with ARS (40 mM).…”

Section: Methodsmentioning

confidence: 99%

“…After infection, P. gingivalis can traverse from ECs to SMCs as the atherosclerotic process progresses (Reyes et al, ). Recently, P. gingivalis infection has been reported to cause aortic intimal hyperplasia in mice (Hokamura et al, ; Liu et al, ; Yang, Guo, Jia, & Jia, ). Moreover, it has also been indicated that the lipopolysaccharide (LPS) and outer membrane vesicles derived from P. gingivalis stimulate the proliferation and calcification of VSMCs (Demer & Tintut, ; Gu et al, ; Kapustin & Shanahan, ; Leopold, ; Yang et al, ).…”

Section: Introductionmentioning

confidence: 99%

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Regulation of calcification in human aortic smooth muscle cells infected with high‐glucose‐treated Porphyromonas gingivalis

Chen

Lin

Chien

et al. 2018

Journal Cellular Physiology

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Porphyromonas (P.) gingivalis infection leading to the periodontitis has been associated with the development of systemic diseases, including cardiovascular diseases and diabetes. However, the effect of a high concentration of glucose (HG) on the invasion efficiency of P. gingivalis and the consequent modulation of pathogenesis in vascular cells, especially in the vascular smooth muscle cells (VSMCs), remains unclear. Hence, the aim of this study was to investigate whether treating P. gingivalis with HG could change its invasion capability and result in VSMC calcification and the underlying mechanism. Human aortic SMCs (HASMCs) and P. gingivalis strain CCUG25226 were used in this study. We found that HGPg infection of HASMCs could initiate the HASMC calcification by stimulating the autocrine regulation of bone morphogenetic protein (BMP) 4 in HASMCs. The upregulation of BMP4 expression in HASMCs was mediated by toll-like receptor 4 and ERK1/2-p38 signaling after P. gingivalis infection. Moreover, the autocrine action of BMP4 in HGPg infection-initiated HASMC calcification upregulated BMP4-specific downstream smad1/5/8-runx2 signaling to increase the expressions of bone-related matrix proteins, that is, osteopontin, osteocalcin, and alkaline phosphatase. This study elucidates the detailed mechanism of HGPg infection-initiated calcification of HASMCs and indicates a possible therapeutic role of BMP4 in P. gingivalis infection-associated vascular calcification.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Regulation of calcification in human aortic smooth muscle cells infected with high‐glucose‐treated Porphyromonas gingivalis

Chen

Lin

Chien

et al. 2018

Journal Cellular Physiology

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“…Fifth, vascular calcification is a prominent feature of AS. P. gingivalis LPS can stimulate the proliferation and calcification of SMCs, resulting in vascular calcification [ 42 ]. P. gingivalis OMVs were also reported to promote vascular SMC calcification through ERK1/2-RUNX2 [ 43 ].…”

Section: Cardiologymentioning

confidence: 99%

Porphyromonas gingivalis and Its Systemic Impact: Current Status

et al. 2020

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The relationship between periodontitis and systemic diseases, notably including atherosclerosis and diabetes, has been studied for several years. Porphyromonas gingivalis, a prominent component of oral microorganism communities, is the main pathogen that causes periodontitis. As a result of the extensive analysis of this organism, the evidence of its connection to systemic diseases has become more apparent over the last decade. A significant amount of research has explored the role of Porphyromonas gingivalis in atherosclerosis, Alzheimer’s disease, rheumatoid arthritis, diabetes, and adverse pregnancy outcomes, while relatively few studies have examined its contribution to respiratory diseases, nonalcoholic fatty liver disease, and depression. Here, we provide an overview of the current state of knowledge about Porphyromonas gingivalis and its systemic impact in an aim to inform readers of the existing epidemiological evidence and the most recent preclinical studies. Additionally, the possible mechanisms by which Porphyromonas gingivalis is involved in the onset or exacerbation of diseases, together with its effects on systemic health, are covered. Although a few results remain controversial, it is now evident that Porphyromonas gingivalis should be regarded as a modifiable factor for several diseases.

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“…P. gingivalis is a gram negative bacterium. Experimental results indicate that P. gingivalis DNA and P. gingivalis endotoxin (LPS) can be found in a therogenic plaque in CVD patients with periodontal disease (Liu et al, ). Lee et al () indicated that P. gingivalis damages H9c2 cardiomyoblasts by inducing hypertrophy markers and activating the MMP 9 fibrosis marker.…”

Section: Introductionmentioning

confidence: 99%

Stem cells rescue cardiomyopathy induced by P. gingivalis‐LPS via miR‐181b

Chen

Battsengel

Kuo

et al. 2018

Journal Cellular Physiology

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Systemic inflammation induced by bacterial infection is one of several causative agents for cardiovascular disorders in patients with periodontal disease. Experimental results indicate that miRNAs play important roles in systemic inflammation induced by endotoxins. Further evidence states that stem cell based therapy shows potential in the treatment of inflammatory responses induced by sepsis. This study investigates if stem cells show protective effects on cardiomyocyte damage induced by porphyromonas gingivalis-LPS (Pg-LPS) through regulating miRNAs. H9c2 cardiomyoblasts and neonatal rat cardiomyocytes (NRCMs) were damaged using Pg-LPS in this study. Pg-LPS damaged H9c2 or NRCMs were then rescued using adipose-derived stem cells (ADSC). The experimental results reveal that Pg-LPS treatment is capable of inducing TLR4/NFκB axis activation, cell death signaling and IGF1R/PI3 K/Akt axis suppression. miR181b was downregulated in Pg-LPS damaged H9c2/NRCMs. All markers were improved in H9c2/NRCMs cocultured with ADSC. miR181b mimic and inhibitor confirmed that miR181b plays a central role in regulating the cardio protective effect on Pg-LPS damaged H9c2/NRCMs cocultured with ADSC. miR181b acts as potential therapeutic marker in cardiomyopathy induced by Pg-LPS. Transplantation of adipose-derived stem cells show potential in the treatment of cardiomyopathy induced by porphyromonas gingivalis endotoxin via regulation of miR181b.

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Porphyromonas gingivalis Lipopolysaccharide Stimulation of Vascular Smooth Muscle Cells Activates Proliferation and Calcification

Abstract: Pg-LPS can stimulate VSMC calcification, which results in vascular calcification, further proving the precise relationship between periodontitis and vascular calcification.

Cited by 20 publications

References 48 publications

Regulation of calcification in human aortic smooth muscle cells infected with high‐glucose‐treated Porphyromonas gingivalis

Regulation of calcification in human aortic smooth muscle cells infected with high‐glucose‐treated Porphyromonas gingivalis

Porphyromonas gingivalis and Its Systemic Impact: Current Status

Stem cells rescue cardiomyopathy induced by P. gingivalis‐LPS via miR‐181b

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