Porphorymonas gingivalis induces intracellular adhesion molecule-1 expression in endothelial cells through the nuclear factor-kappaB pathway, but not through the p38 MAPK pathway

Zhang, D.; Zheng, Haixue; Zhao, Jie; Li, Lin; Li, C.; Liu, J.; Pan, Yaping

doi:10.1111/j.1600-0765.2010.01305.x

Cited by 25 publications

(35 citation statements)

References 37 publications

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“…NF-κBIZ in particular demonstrated a marked 11.2-fold and 9.6-fold up-regulation, at 6 h and 24 h, respectively. The present findings are in agreement with previous studies demonstrating a central role of NF-κB in the pro-inflammatory responses to P. gingivalis in various cell types including fibroblasts, stromal cells, gingival epithelial cells, osteoblasts, cementoblasts and endothelial cells [11], [90], [93], [110]–[112].…”

Section: Resultssupporting

confidence: 94%

Transcriptional Profiling of Bone Marrow Stromal Cells in Response to Porphyromonas gingivalis Secreted Products

Reddi

Belibasakis

2012

PLoS ONE

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Periodontitis is an infectious inflammatory disease that destroys the tooth-supporting (periodontal) tissues. Porphyromonas gingivalis is an oral pathogen highly implicated in the pathogenesis of this disease. It can exert its effects to a number of cells, including osteogenic bone marrow stromal cells which are important for homeostastic capacity of the tissues. By employing gene microarray technology, this study aimed to describe the overall transcriptional events (>2-fold regulation) elicited by P. gingivalis secreted products in bone marrow stromal cells, and to dissect further the categories of genes involved in bone metabolism, inflammatory and immune responses. After 6 h of challenge with P. gingivalis, 271 genes were up-regulated whereas 209 genes were down-regulated, whereas after 24 h, these numbers were 259 and 109, respectively. The early (6 h) response was characterised by regulation of genes associated with inhibition of cell cycle, induction of apoptosis and loss of structural integrity, whereas the late (24 h) response was characterised by induction of chemokines, cytokines and their associated intracellular pathways (such as NF-κB), mediators of connective tissue and bone destruction, and suppression of regulators of osteogenic differentiation. The most strongly up-regulated genes were lipocalin 2 (LCN2) and serum amyloid A3 (SAA3), both encoding for proteins of the acute phase inflammatory response. Collectively, these transcriptional changes elicited by P. gingivalis denote that the fundamental cellular functions are hindered, and that the cells acquire a phenotype commensurate with propagated innate immune response and inflammatory-mediated tissue destruction. In conclusion, the global transcriptional profile of bone marrow stromal cells in response to P. gingivalis is marked by deregulated homeostatic functions, with implications in the pathogenesis of periodontitis.

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Section: Resultssupporting

confidence: 94%

Transcriptional Profiling of Bone Marrow Stromal Cells in Response to Porphyromonas gingivalis Secreted Products

Reddi

Belibasakis

2012

PLoS ONE

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“…In preparation for this study, we ran experiments with MOIs of 10, 100, and 1,000 (data not shown). Results of studies using various MOIs, including the MOIs of 10 (18), 100 (19,20), and 1,000 (18), have been previously reported in the literature. The optimum concentration achieved in our experiments-in line with most publications in the literature-was the MOI of 100.…”

Section: Methodsmentioning

confidence: 89%

Endothelial Cell Response to Fusobacterium nucleatum

Mendes

Nguyen²,

Stephens³

et al. 2016

Infect Immun

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c Vascular response is an essential aspect of an effective immune response to periodontal disease pathogens, as new blood vessel formation contributes to wound healing and inflammation. Gaining a greater understanding of the factors that affect vascular response may then contribute to future breakthroughs in dental medicine. In this study, we have characterized the endothelial cell response to the common bacterium Fusobacterium nucleatum, an important bridging species that facilitates the activity of late colonizers of the dental biofilm. Endothelial cells were infected with Fusobacterium nucleatum (strain 25586) for periods of 4, 12, 24, or 48 h. Cell proliferation and tube formation were analyzed, and expression of adhesion molecules (CD31 and CD34) and vascular endothelial growth factor (VEGF) receptors 1 and 2 was measured by fluorescenceactivated cell sorter (FACS) analysis. Data indicate that F. nucleatum impaired endothelial cell proliferation and tube formation. The findings suggest that the modified endothelial cell response acts as a mechanism promoting the pathogenic progression of periodontal diseases and may potentially suggest the involvement of periodontopathogens in systemic diseases associated with periodontal inflammation.

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“…At present, several signaling pathways have been shown to be involved in osteogenesis, such as MAPKs, BMP-2-Smad and NF-κB [21–23]. Among them, p38 and ERK1/2 MAPKs have been reported to be important for early osteoblast differentiation in various cell lines [24].…”

Section: Resultsmentioning

confidence: 99%

A Specific Oligodeoxynucleotide Promotes the Differentiation of Osteoblasts via ERK and p38 MAPK Pathways

Shen

Zhang

et al. 2012

IJMS

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A specific oligodeoxynucleotide (ODN), ODN MT01, was found to have positive effects on the proliferation and activation of the osteoblast-like cell line MG 63. In this study, the detailed signaling pathways in which ODN MT01 promoted the differentiation of osteoblasts were systematically examined. ODN MT01 enhanced the expression of osteogenic marker genes, such as osteocalcin and type I collagen. Furthermore, ODN MT01 activated Runx2 phosphorylation via ERK1/2 mitogen-activated protein kinase (MAPK) and p38 MAPK. Consistently, ODN MT01 induced up-regulation of osteocalcin, alkaline phosphatase (ALP) and type I collagen, which was inhibited by pre-treatment with the ERK1/2 inhibitor U0126 and the p38 inhibitor SB203580. These results suggest that the ERK1/2 and p38 MAPK pathways, as well as Runx2 activation, are involved in ODN MT01-induced up-regulation of osteocalcin, type I collagen and the activity of ALP in MG 63 cells.

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Porphorymonas gingivalis induces intracellular adhesion molecule-1 expression in endothelial cells through the nuclear factor-kappaB pathway, but not through the p38 MAPK pathway

Abstract: The induction of ICAM-1 by infection of umbilical vein endothelial cells with P. gingivalis might be mediated through the NF-κB pathway, but not by the p38 MAPK pathway.

Cited by 25 publications

References 37 publications

Transcriptional Profiling of Bone Marrow Stromal Cells in Response to Porphyromonas gingivalis Secreted Products

Transcriptional Profiling of Bone Marrow Stromal Cells in Response to Porphyromonas gingivalis Secreted Products

Endothelial Cell Response to Fusobacterium nucleatum

A Specific Oligodeoxynucleotide Promotes the Differentiation of Osteoblasts via ERK and p38 MAPK Pathways

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