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Involvement of interleukin-23 induced by Porphyromonas endodontalis lipopolysaccharide in osteoclastogenesis
by
Yang, Di
, Ma, Nan
, Okamura, Hirohiko
, Haneji, Tatsuji
, Qiu, Lihong
, Teramachi, Jumpei
, Hasegawa, Tomokazu
in
Alveolar bone
/ Animals
/ Bone cells
/ Bone loss
/ Bone turnover
/ Care and treatment
/ Chromones - pharmacology
/ Cytokines
/ Endodontics
/ Gene expression
/ Health aspects
/ Humans
/ Immunohistochemistry
/ Inflammation
/ Interleukin 23
/ Interleukin-23 - antagonists & inhibitors
/ Interleukin-23 - genetics
/ Interleukin-23 - metabolism
/ Interleukins
/ Kinases
/ lipopolysaccharide
/ Lipopolysaccharides
/ Lipopolysaccharides - toxicity
/ Mice
/ Microorganisms
/ Morpholines - pharmacology
/ NF-kappa B - antagonists & inhibitors
/ NF-kappa B - metabolism
/ NFATC Transcription Factors - metabolism
/ Nitriles - pharmacology
/ Osteoblasts - cytology
/ Osteoblasts - drug effects
/ Osteoblasts - metabolism
/ Osteoclastogenesis
/ Osteogenesis - drug effects
/ Pathogenesis
/ Periodontal ligament
/ periodontal ligament cells
/ Periodontitis - diagnosis
/ Periodontitis - metabolism
/ Periodontitis - pathology
/ Phosphatidylinositol 3-Kinases - antagonists & inhibitors
/ Phosphatidylinositol 3-Kinases - metabolism
/ Polymerase chain reaction
/ Porphyromonas endodontalis
/ Porphyromonas endodontalis - metabolism
/ Proto-Oncogene Proteins c-fos - metabolism
/ RANK Ligand - pharmacology
/ RAW 264.7 Cells
/ Reverse transcription
/ RNA Interference
/ RNA, Small Interfering - metabolism
/ Rodents
/ Root canal therapy
/ Root canals
/ Studies
/ Sulfones - pharmacology
/ Transcription factors
/ Virulence factors
2017
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Involvement of interleukin-23 induced by Porphyromonas endodontalis lipopolysaccharide in osteoclastogenesis
by
Yang, Di
, Ma, Nan
, Okamura, Hirohiko
, Haneji, Tatsuji
, Qiu, Lihong
, Teramachi, Jumpei
, Hasegawa, Tomokazu
in
Alveolar bone
/ Animals
/ Bone cells
/ Bone loss
/ Bone turnover
/ Care and treatment
/ Chromones - pharmacology
/ Cytokines
/ Endodontics
/ Gene expression
/ Health aspects
/ Humans
/ Immunohistochemistry
/ Inflammation
/ Interleukin 23
/ Interleukin-23 - antagonists & inhibitors
/ Interleukin-23 - genetics
/ Interleukin-23 - metabolism
/ Interleukins
/ Kinases
/ lipopolysaccharide
/ Lipopolysaccharides
/ Lipopolysaccharides - toxicity
/ Mice
/ Microorganisms
/ Morpholines - pharmacology
/ NF-kappa B - antagonists & inhibitors
/ NF-kappa B - metabolism
/ NFATC Transcription Factors - metabolism
/ Nitriles - pharmacology
/ Osteoblasts - cytology
/ Osteoblasts - drug effects
/ Osteoblasts - metabolism
/ Osteoclastogenesis
/ Osteogenesis - drug effects
/ Pathogenesis
/ Periodontal ligament
/ periodontal ligament cells
/ Periodontitis - diagnosis
/ Periodontitis - metabolism
/ Periodontitis - pathology
/ Phosphatidylinositol 3-Kinases - antagonists & inhibitors
/ Phosphatidylinositol 3-Kinases - metabolism
/ Polymerase chain reaction
/ Porphyromonas endodontalis
/ Porphyromonas endodontalis - metabolism
/ Proto-Oncogene Proteins c-fos - metabolism
/ RANK Ligand - pharmacology
/ RAW 264.7 Cells
/ Reverse transcription
/ RNA Interference
/ RNA, Small Interfering - metabolism
/ Rodents
/ Root canal therapy
/ Root canals
/ Studies
/ Sulfones - pharmacology
/ Transcription factors
/ Virulence factors
2017
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Involvement of interleukin-23 induced by Porphyromonas endodontalis lipopolysaccharide in osteoclastogenesis
by
Yang, Di
, Ma, Nan
, Okamura, Hirohiko
, Haneji, Tatsuji
, Qiu, Lihong
, Teramachi, Jumpei
, Hasegawa, Tomokazu
in
Alveolar bone
/ Animals
/ Bone cells
/ Bone loss
/ Bone turnover
/ Care and treatment
/ Chromones - pharmacology
/ Cytokines
/ Endodontics
/ Gene expression
/ Health aspects
/ Humans
/ Immunohistochemistry
/ Inflammation
/ Interleukin 23
/ Interleukin-23 - antagonists & inhibitors
/ Interleukin-23 - genetics
/ Interleukin-23 - metabolism
/ Interleukins
/ Kinases
/ lipopolysaccharide
/ Lipopolysaccharides
/ Lipopolysaccharides - toxicity
/ Mice
/ Microorganisms
/ Morpholines - pharmacology
/ NF-kappa B - antagonists & inhibitors
/ NF-kappa B - metabolism
/ NFATC Transcription Factors - metabolism
/ Nitriles - pharmacology
/ Osteoblasts - cytology
/ Osteoblasts - drug effects
/ Osteoblasts - metabolism
/ Osteoclastogenesis
/ Osteogenesis - drug effects
/ Pathogenesis
/ Periodontal ligament
/ periodontal ligament cells
/ Periodontitis - diagnosis
/ Periodontitis - metabolism
/ Periodontitis - pathology
/ Phosphatidylinositol 3-Kinases - antagonists & inhibitors
/ Phosphatidylinositol 3-Kinases - metabolism
/ Polymerase chain reaction
/ Porphyromonas endodontalis
/ Porphyromonas endodontalis - metabolism
/ Proto-Oncogene Proteins c-fos - metabolism
/ RANK Ligand - pharmacology
/ RAW 264.7 Cells
/ Reverse transcription
/ RNA Interference
/ RNA, Small Interfering - metabolism
/ Rodents
/ Root canal therapy
/ Root canals
/ Studies
/ Sulfones - pharmacology
/ Transcription factors
/ Virulence factors
2017
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Involvement of interleukin-23 induced by Porphyromonas endodontalis lipopolysaccharide in osteoclastogenesis
Journal Article
Involvement of interleukin-23 induced by Porphyromonas endodontalis lipopolysaccharide in osteoclastogenesis
2017
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Overview
Periapical lesions are characterized by the destruction of periapical bone, and occur as a result of local inflammatory responses to root canal infection by microorganisms including Porphyromonas endodontalis (P. endodontalis). P. endodontalis and its primary virulence factor, lipopolysaccharide (LPS), are associated with the development of periapical lesions and alveolar bone loss. Interleukin-23 (IL-23) is critical in the initiation and progression of periodontal disease via effects on peripheral bone metabolism. The present study investigated the expression of IL-23 in tissue where a periapical lesion was present, and the effect of P. endodontalis LPS on the expression of IL-23 in periodontal ligament (PDL) cells. Reverse transcription- quantitative polymerase chain reaction and immunohistochemistry revealed increased levels of IL-23 expression in tissue with periapical lesions compared with healthy PDL tissue. Treatment with P. endodontalis LPS increased the expression of IL-23 in the SH-9 human PDL cell line. BAY11-7082, a nuclear factor κB inhibitor, suppressed P. endodontalis LPS-induced IL-23 expression in SH-9 cells. Treatment of RAW264.7 cells with conditioned medium from P. endodontalis LPS-treated SH-9 cells promoted osteoclastogenesis. By contrast, RAW264.7 cells treated with conditioned medium from IL-23-knockdown SH-9 cells underwent reduced levels of osteoclastogenesis. The results of the present study indicated that the expression of IL-23 in PDL cells induced by P. endodontalis LPS treatment may be involved in the progression of periapical lesions via stimulation of the osteoclastogenesis process.
Publisher
D.A. Spandidos,Spandidos Publications,Spandidos Publications UK Ltd
Subject
/ Animals
/ Humans
/ Interleukin-23 - antagonists & inhibitors
/ Kinases
/ Lipopolysaccharides - toxicity
/ Mice
/ NF-kappa B - antagonists & inhibitors
/ NFATC Transcription Factors - metabolism
/ Phosphatidylinositol 3-Kinases - antagonists & inhibitors
/ Phosphatidylinositol 3-Kinases - metabolism
/ Porphyromonas endodontalis - metabolism
/ Proto-Oncogene Proteins c-fos - metabolism
/ RNA, Small Interfering - metabolism
/ Rodents
/ Studies
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