+ Site Statistics
References:
54,258,434
Abstracts:
29,560,870
PMIDs:
28,072,757
+ Search Articles
+ PDF Full Text Service
How our service works
Request PDF Full Text
+ Follow Us
Follow on Facebook
Follow on Twitter
Follow on LinkedIn
+ Subscribe to Site Feeds
Most Shared
PDF Full Text
+ Translate
+ Recently Requested

A Novel Cartilage Fragments Stimulation Model Revealed that Macrophage Inflammatory Response Causes an Upregulation of Catabolic Factors of Chondrocytes In Vitro



A Novel Cartilage Fragments Stimulation Model Revealed that Macrophage Inflammatory Response Causes an Upregulation of Catabolic Factors of Chondrocytes In Vitro



Cartilage 2019: 1947603519828426



Osteoarthritis is a progressive joint disease characterized by cartilage degradation and synovial inflammation. Presence of cartilage fragments in the joint due to degradation of cartilage is thought to be associated with local inflammatory response and progressive osteoarthritic process. Understanding the mechanism by which cartilage fragments elicit this destructive process should aid in designing novel therapeutic approaches. Therefore, objective of current study is to establish an in vitro model to examine the cross-talk between chondrocytes and cartilage fragments-stimulated macrophages. Cartilage fragments were prepared from femoral head cartilages of mice and analyzed using a scanning electron microscope and particle size analyzer. Bone marrow-derived macrophages were co-cultured with cartilage fragments and chondrocytes using transwell co-culture system. Macrophage inflammatory mediators in supernatant of cultures were determined by ELISA and gene expression of macrophages and chondrocyte were quantified by qRT-PCR. Shapes of cartilage fragments were irregular with sizes ranged between 0.54 and 55 μm. Macrophages cultured with cartilage fragments released significantly higher concentrations of TNF-α, IL-6, and NO than those of mock and control. Consistently, gene expressions of TNF-α, IL-6, and MMP-9 were significantly increased in stimulated macrophages. The elevation in production of pro-inflammatory molecules in stimulated macrophages cultures were coincident with an increase in gene expression of chondrocyte MMP-13, iNOS, and IL-6. We developed an in vitro co-culture model to study the impact of stimulation of macrophage by cartilage fragments on the expression of chondrocyte carbolic factors. Our results revealed that cartilage fragments triggered macrophages inflammatory response that enhanced the production of chondrocyte catabolic factors.

Please choose payment method:






(PDF emailed within 0-6 h: $19.90)

Accession: 066446402

Download citation: RISBibTeXText

PMID: 30704288

DOI: 10.1177/1947603519828426


Related references

Carnosol Inhibits Pro-Inflammatory and Catabolic Mediators of Cartilage Breakdown in Human Osteoarthritic Chondrocytes and Mediates Cross-Talk between Subchondral Bone Osteoblasts and Chondrocytes. Plos One 10(8): E0136118, 2016

Paracrine interactions of chondrocytes and macrophages in cartilage degradation: articular chondrocytes provide factors that activate macrophage-derived pro-gelatinase B (pro-MMP-9). Journal of Cell Science 114(Pt 21): 3813-3822, 2001

IL37 suppresses IL-1β-induced pro-inflammatory cytokine and catabolic enzyme production in primary human oa chondrocytes: protection against cartilage degradation. Osteoarthritis and Cartilage 24: S336-S337, 2016

Stimulation of inflammatory gene expression in human preadipocytes by macrophage-conditioned medium: upregulation of IL-6 production by macrophage-derived IL-1β. Molecular and Cellular Endocrinology 349(2): 239-247, 2012

Rebamipide attenuates pain severity and cartilage degeneration in a rat model of osteoarthritis by downregulating oxidative damage and catabolic activity in chondrocytes. Osteoarthritis and Cartilage 20(11): 1426-1438, 2013

AB0141Rebamipide attenuates pain severity and cartilage degeneration in a rat model of osteoarthritis by downregulating oxidative damage and catabolic activity in chondrocytes. Annals of the Rheumatic Diseases 71(Suppl 3): 645.14-645, 2013

Effects of Anti-Inflammatory Agents on Expression of Early Responsive Inflammatory and Catabolic Genes in Ex Vivo Porcine Model of Acute Knee Cartilage Injury. Cartilage 9(3): 293-303, 2018

Adipose-derived stem cells induce autophagic activation and inhibit catabolic response to pro-inflammatory cytokines in rat chondrocytes. Osteoarthritis and Cartilage 24(6): 1071-1081, 2018

Freshly isolated osteoarthritic chondrocytes are catabolically more active than normal chondrocytes, but less responsive to catabolic stimulation with interleukin-1beta. Arthritis and Rheumatism 52(1): 136-143, 2005

OA cartilage derived chondrocytes encapsulated in poly(ethylene glycol) diacrylate (PEGDA) for the evaluation of cartilage restoration and apoptosis in an in vitro model. Histology and Histopathology 26(10): 1265-1278, 2011

Cordycepin modulates inflammatory and catabolic gene expression in interleukin-1beta-induced human chondrocytes from advanced-stage osteoarthritis: an in vitro study. International Journal of Clinical and Experimental Pathology 7(10): 6575-6584, 2015

Matrix metalloproteinase inhibitor CGS 27023A protects COMP and proteoglycan in the bovine articular cartilage but not the release of their fragments from cartilage after prolonged stimulation in vitro with IL-1 alpha. Annals of the New York Academy of Sciences 878: 607-611, 1999

Periodic Nanomechanical Stimulation in a Biokinetics Model Identifying Anabolic and Catabolic Pathways Associated With Cartilage Matrix Homeostasis. Journal of Nanotechnology in Engineering and Medicine 1(4), 2010

A Distinct Catabolic to Anabolic Threshold Due to Single-Cell Static Nanomechanical Stimulation in a Cartilage Biokinetics Model. Journal of Nanotechnology in Engineering and Medicine 1(3), 2010

Chondrocytes from osteoarthritis cartilage show an altered electrophysiological response to mechanical stimulation. Journal of Pathology 184(SUPPL ): 37A, 1998