Lorenz, J. and Schaefer, N. and Bauer, R. and Jenei-Lanzl, Z. and Springorum, R. H. and Graessel, S. (2016) Norepinephrine modulates osteoarthritic chondrocyte metabolism and inflammatory responses. OSTEOARTHRITIS AND CARTILAGE, 24 (2). pp. 325-334. ISSN 1063-4584, 1522-9653
Full text not available from this repository. (Request a copy)Abstract
Objective: Norepinephrine (NE) was measured in synovial fluid of trauma patients and sympathetic nerve fibers were detected in healthy and osteoarthritic (OA) joint tissues indicating that cartilage pathophysiology might be influenced by sympathetic neurotransmitters. The aim of this study was to elucidate the mostly unknown role of NE in OA chondrocyte metabolism and inflammatory responses. Methods: Articular cartilage was received after total knee replacement surgery from OA patients. Expression of adrenergic receptors (AR) and tyrosine hydroxylase (TH) was tested with end point polymerase chain reaction (PCR) and immunohistochemistry. 3-dimensional (3D) cell cultures were employed to analyze effects of NE on chondrocyte cell metabolism and the expression of interleukins (ILs), matrix metalloproteases (MMPs), tissue inhibitor of metalloproteases (TIMPs), glycosaminoglycan (GAG) and collagen II under non- and inflammatory conditions. Chondrocyte monolayer cultures were used to specify AR subtypes, to analyze cell cycle distribution and to determine catecholamines in cell culture supernatants. Results: AR subtypes and TH were detected in chondrocytes, whereas NE was not released in measurable amounts. 10(-6) M NE reversed IL-1 beta induced changes in IL-8, MMP-13, GAG and collagen II expression/production indicating for beta-AR signaling. Additionally, NE caused cell cycle slow down and decreased proliferation via beta-AR signaling. 10(-8) M NE increased the number of proliferating cells and induced apoptosis via alpha 1-AR signaling. Conclusions: NE affects chondrocytes from OA cartilage regarding inflammatory response and its cell metabolism in a dose dependent manner. The sympathetic nervous system (SNS) may have a dual function in OA pathology with preserving a stable chondrocyte phenotype via beta-AR signaling and OA pathogenesis accelerating effects via alpha-AR signaling. (C) 2015 Osteoarthritis Research Society International. Published by Elsevier Ltd. All rights reserved.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | SYMPATHETIC-NERVE FIBERS; CHONDROGENIC DIFFERENTIATION; ARTICULAR CHONDROCYTES; SUBSTANCE-P; STEM-CELLS; CARTILAGE; EXPRESSION; BONE; APOPTOSIS; RECEPTORS; Osteoarthritis; Articular chondrocytes; Norepinephrine; IL-1 beta; Sympathetic nervous system |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Innere Medizin I Medicine > Lehrstuhl für Orthopädie |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 14 Mar 2019 10:29 |
| Last Modified: | 14 Mar 2019 10:29 |
| URI: | https://pred.uni-regensburg.de/id/eprint/2497 |
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