Abstract
BackgroundThe influence of the sympathetic nervous system (SNS) on metabolism of bone and cartilage expressing β-adrenergic receptors (AR) was suggested. Here, we investigated whether the SNS functions as a modulator of cartilage metabolism induced by interleukin-1beta (IL-1β).MethodsHuman articular chondrocytes and articular cartilage were collected from patients with osteoarthritis (OA). Chondrocyte monolayer and cartilage explant culture were stimulated with IL-1β. The activity of β-ARs was modulated by an agonist, norepinephrine (NE), and antagonists, including propranolol, atenolol, nebivolol, and nadolol.ResultsThe levels of β1-, β2-, and β3-AR in OA cartilage and IL-1β-treated chondrocytes were lower than normal cartilage and untreated cells. Treatment of chondrocytes with IL-1β and β-blockers, including propranolol, atenolol, nebivolol, and nadolol, for 6 h significantly upregulated IL-1β-induced expression of MMP-1, -3, and − 13, compared to chondrocytes treated with IL-1β alone, indicating that antagonism of β-AR confers catabolic signals. On the other hand, NE antagonized IL-1β-induced catabolic response. In addition, NE significantly inhibited IL-1β-induced release of glycosaminoglycan (GAG) from cartilage explant culture. In addition, β-AR activity significantly affected IL-1β-stimulated phosphorylation of JNK and ERK. These results indicate that β-AR signal is associated with cartilage metabolism.ConclusionsOur findings showed that β-ARs is a regulator of cartilage catabolism induced with IL-1β.
Highlights
The influence of the sympathetic nervous system (SNS) on metabolism of bone and cartilage expressing β-adrenergic receptors (AR) was suggested
The mRNA expression level of β1, β2, and β3-AR in normal cartilages varied depending on the donor, it was significantly lower in OA cartilage (Fig. 1A)
The level of β-ARs is reduced in chondrocytes in response to IL-1β To examine the effect of IL-1β on expression of β-ARs, chondrocytes were exposed to IL-1β (1 ng/ml) for 72 h
Summary
The influence of the sympathetic nervous system (SNS) on metabolism of bone and cartilage expressing β-adrenergic receptors (AR) was suggested. We investigated whether the SNS functions as a modulator of cartilage metabolism induced by interleukin-1beta (IL-1β). Synthesis of extracellular matrix (ECM) in chondrocytes is maintained by balance of anabolic factors and catabolic factors, such as matrix metalloproteinases (MMPs), and are Stimuli from inflammation and mechanical stress are detected by sensory nerve fibers and is transmitted to the central nervous system, which subsequently activates the sympathetic nervous system (SNS). A series of processes, including release of neurotransmitter such as norepinephrine (NE), lymphocyte recruitment, and increase of blood and lymph flow, are induced at the site of inflammation [3]. The sympathetic nerve fibers expressing α- and β-adrenergic receptors (AR) are found in various tissues, including synovium and bone.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
