TNF alpha contributes for attenuating both Y(397)FAK and Y(416)Src phosphorylations in osteoblasts

A. D. M. Cavagis; E. R. Takamori; J. M. Granjeiro; R. C. Oliveira; C. V. Ferreira; M. P. Peppelenbosch; W. F. Zambuzzi

doi:10.1111/odi.12202

TNF alpha contributes for attenuating both Y(397)FAK and Y(416)Src phosphorylations in osteoblasts

A. D. M. Cavagis, E. R. Takamori, J. M. Granjeiro, R. C. Oliveira, C. V. Ferreira, M. P. Peppelenbosch, W. F. Zambuzzi^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › Academic › peer-review

19 Citations (Scopus)

Abstract

ObjectiveOur poor understanding of how inflammatory mediators can affect osteoblast behavior led us to investigate the tumor necrosis factor (TNF)-induced focal adhesion kinase (FAK) and Src phosphorylation.

Material and MethodsMC3T3-E1 pre-osteoblast cells were harvested at specific time points after either TNF treatment or RAW267 stimulated conditioned medium, and thereafter cell extracts were prepared for Immunoblotting assay. ELISA detected TNF content at conditioned medium. Tumor necrosis factor--neutralizing antibodies also were used.

ResultsIt was possible to show that TNF provokes attenuation at Y-phosphorylation of both FAK (at Y-397) and Src (at Y-416) proteins (P

ConclusionsAltogether, these results suggest that LPS-stimulated macrophage mediators attenuate both FAK and Src activations in osteoblast, suggesting a novel role for TNF on osteoblast performance.

Original language	English
Pages (from-to)	780-786
Number of pages	7
Journal	Oral diseases
Volume	20
Issue number	8
DOIs	https://doi.org/10.1111/odi.12202
Publication status	Published - Nov-2014

Keywords

cell signaling
focal adhesion kinase
inflammation
Lipopolysaccharide
macrophages
osteoblasts
periodontal disease
Src
tumor necrosis factor
NECROSIS-FACTOR-ALPHA
FOCAL ADHESION KINASE
DEPENDENT EFFECTOR MECHANISM
ACTIVATED PROTEIN-KINASE
OSTEOGENESIS IN-VITRO
NF-KAPPA-B
SIGNALING PATHWAYS
DIFFERENTIATION
IDENTIFICATION
MACROPHAGES

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@article{27ff0e0d4acb4873987423ae5f773c94,

title = "TNF alpha contributes for attenuating both Y(397)FAK and Y(416)Src phosphorylations in osteoblasts",

abstract = "ObjectiveOur poor understanding of how inflammatory mediators can affect osteoblast behavior led us to investigate the tumor necrosis factor (TNF)-induced focal adhesion kinase (FAK) and Src phosphorylation.Material and MethodsMC3T3-E1 pre-osteoblast cells were harvested at specific time points after either TNF treatment or RAW267 stimulated conditioned medium, and thereafter cell extracts were prepared for Immunoblotting assay. ELISA detected TNF content at conditioned medium. Tumor necrosis factor--neutralizing antibodies also were used.ResultsIt was possible to show that TNF provokes attenuation at Y-phosphorylation of both FAK (at Y-397) and Src (at Y-416) proteins (PConclusionsAltogether, these results suggest that LPS-stimulated macrophage mediators attenuate both FAK and Src activations in osteoblast, suggesting a novel role for TNF on osteoblast performance.",

keywords = "cell signaling, focal adhesion kinase, inflammation, Lipopolysaccharide, macrophages, osteoblasts, periodontal disease, Src, tumor necrosis factor, NECROSIS-FACTOR-ALPHA, FOCAL ADHESION KINASE, DEPENDENT EFFECTOR MECHANISM, ACTIVATED PROTEIN-KINASE, OSTEOGENESIS IN-VITRO, NF-KAPPA-B, SIGNALING PATHWAYS, DIFFERENTIATION, IDENTIFICATION, MACROPHAGES",

author = "Cavagis, {A. D. M.} and Takamori, {E. R.} and Granjeiro, {J. M.} and Oliveira, {R. C.} and Ferreira, {C. V.} and Peppelenbosch, {M. P.} and Zambuzzi, {W. F.}",

year = "2014",

month = nov,

doi = "10.1111/odi.12202",

language = "English",

volume = "20",

pages = "780--786",

journal = "Oral diseases",

issn = "1354-523X",

publisher = "Wiley",

number = "8",

}

TY - JOUR

T1 - TNF alpha contributes for attenuating both Y(397)FAK and Y(416)Src phosphorylations in osteoblasts

AU - Cavagis, A. D. M.

AU - Takamori, E. R.

AU - Granjeiro, J. M.

AU - Oliveira, R. C.

AU - Ferreira, C. V.

AU - Peppelenbosch, M. P.

AU - Zambuzzi, W. F.

PY - 2014/11

Y1 - 2014/11

N2 - ObjectiveOur poor understanding of how inflammatory mediators can affect osteoblast behavior led us to investigate the tumor necrosis factor (TNF)-induced focal adhesion kinase (FAK) and Src phosphorylation.Material and MethodsMC3T3-E1 pre-osteoblast cells were harvested at specific time points after either TNF treatment or RAW267 stimulated conditioned medium, and thereafter cell extracts were prepared for Immunoblotting assay. ELISA detected TNF content at conditioned medium. Tumor necrosis factor--neutralizing antibodies also were used.ResultsIt was possible to show that TNF provokes attenuation at Y-phosphorylation of both FAK (at Y-397) and Src (at Y-416) proteins (PConclusionsAltogether, these results suggest that LPS-stimulated macrophage mediators attenuate both FAK and Src activations in osteoblast, suggesting a novel role for TNF on osteoblast performance.

AB - ObjectiveOur poor understanding of how inflammatory mediators can affect osteoblast behavior led us to investigate the tumor necrosis factor (TNF)-induced focal adhesion kinase (FAK) and Src phosphorylation.Material and MethodsMC3T3-E1 pre-osteoblast cells were harvested at specific time points after either TNF treatment or RAW267 stimulated conditioned medium, and thereafter cell extracts were prepared for Immunoblotting assay. ELISA detected TNF content at conditioned medium. Tumor necrosis factor--neutralizing antibodies also were used.ResultsIt was possible to show that TNF provokes attenuation at Y-phosphorylation of both FAK (at Y-397) and Src (at Y-416) proteins (PConclusionsAltogether, these results suggest that LPS-stimulated macrophage mediators attenuate both FAK and Src activations in osteoblast, suggesting a novel role for TNF on osteoblast performance.

KW - cell signaling

KW - focal adhesion kinase

KW - inflammation

KW - Lipopolysaccharide

KW - macrophages

KW - osteoblasts

KW - periodontal disease

KW - Src

KW - tumor necrosis factor

KW - NECROSIS-FACTOR-ALPHA

KW - FOCAL ADHESION KINASE

KW - DEPENDENT EFFECTOR MECHANISM

KW - ACTIVATED PROTEIN-KINASE

KW - OSTEOGENESIS IN-VITRO

KW - NF-KAPPA-B

KW - SIGNALING PATHWAYS

KW - DIFFERENTIATION

KW - IDENTIFICATION

KW - MACROPHAGES

U2 - 10.1111/odi.12202

DO - 10.1111/odi.12202

M3 - Article

SN - 1354-523X

VL - 20

SP - 780

EP - 786

JO - Oral diseases

JF - Oral diseases

IS - 8

ER -

TNF alpha contributes for attenuating both Y(397)FAK and Y(416)Src phosphorylations in osteoblasts

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Keywords

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