TLR-2-mediated induction of vascular endothelial growth factor (VEGF) in cartilage in septic joint disease.

TLR-2-mediated induction of vascular endothelial growth factor (VEGF) in cartilage in septic joint disease. Research Abstract Details 

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TLR-2-mediated induction of vascular endothelial growth factor (VEGF) in cartilage in septic joint disease. Abstract Text:

D Varoga,F Paulsen,R Mentlein,J Fay,B Kurz,R ,C Wruck,M B Goldring,T Pufe,

Bacterial arthritis is a progressive joint disease which includes rapid destruction of articular cartilage even after clearance of the causal factor. The resulting post-infectious arthropathy is mainly characterized by self-perpetuating joint destruction and extensive angiogenesis in the emerging pannus-like synovial membrane, but the underlying molecular mechanisms of the bacteria-initiated process remain incompletely understood. This study was conducted to elucidate the expression and regulation of angiogenic and cartilage-destructive vascular endothelial growth factor (VEGF) in septic arthritis. For that purpose, aspirates of synovial fluid from patients with pyogenic arthritis were examined for VEGF levels by ELISA. In vitro studies with primary and immortalized chondrocytes were performed to determine whether Gram-positive and Gram-negative bacteria induce VEGF expression, by using real-time RT-PCR, ELISA, and immunohistochemistry. Activation of the transcription factor AP-1 was assessed by EMSA experiments. The necessity of the Toll-like receptor-2 (TLR-2), ERK-1/-2, and AP-1 pathway for infectious VEGF induction in chondrocytes was examined by using specific blocking reagents. ELISA experiments revealed that aspirates of synovial fluid from patients with pyogenic arthritis contain elevated levels of VEGF. The in vitro results confirmed the transcriptional induction of VEGF in chondrocytes after bacterial challenge by real-time RT-PCR, ELISA, and immunohistochemistry. This activation was mediated by a TLR-2-, ERK-1/-2-, and AP-1-dependent pathway. The findings demonstrate the expression of Toll-like receptors on mesenchymal articular chondrocytes and reveal TLR-2-mediated VEGF induction in human chondrocytes after Gram-positive bacterial sensing. Since VEGF is a potent angiogenic and tissue remodelling factor, evidence that Toll-like receptors contribute to destructive arthropathy after microbial joint infection is provided. VEGF may be a therapeutic target in the future for the prevention of post-infectious cartilage degradation in articular joints.

TLR-2-mediated induction of vascular endothelial growth factor (VEGF) in cartilage in septic joint disease. Publishing Authors By Initials

D Varoga,F Paulsen,R Mentlein,J Fay,B Kurz,R ,C Wruck,MB Goldring,T Pufe,

For similar peptides: intercellular signaling peptides and proteins: angiogenic proteins: vascular endothelial growth factors: vascular endothelial growth factor a research abstracts see: peptides: intercellular signaling peptides and proteins: angiogenic proteins: vascular endothelial growth factors: vascular endothelial growth factor a research

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MEDLINE DATE:

TLR-2-mediated induction of vascular endothelial growth factor (VEGF) in cartilage in septic joint disease. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The Journal of pathology

VOLUME: 210

Page Numbers: 315-24

Journal Abbreviation: J. Pathol.

ISSN: 0022-3417

DAY: 3

MONTH: Nov

YEAR: 2006

TLR-2-mediated induction of vascular endothelial growth factor (VEGF) in cartilage in septic joint disease. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 204634

TLR-2-mediated induction of vascular endothelial growth factor (VEGF) in cartilage in septic joint disease. Keywords Mesh Terms:

KEYWORDS: Vascular Endothelial Growth Factor A

MESH TERMS: metabolism

Chemical & Substance for Abstract: TLR-2-mediated induction of vascular endothelial growth factor (VEGF) in cartilage in septic joint disease. Information

Substance Name: Mitogen-Activated Protein Kinase 3

Registry Number: EC 2.7.1.37

Grant and Affiliation Information for TLR-2-mediated induction of vascular endothelial growth factor (VEGF) in cartilage in septic joint disease.

AFFILIATION: Department of Orthopaedic Trauma Surgery, University Hospital Schleswig-Holstein, Campus Kiel, Germany. deikevaroga@hotmail.com

Country: England

AGENCY: United States NIAMS

GRANT: R01AR45378

ACRONYM: AR

MEDLINETA: J Pathol

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