CCL22 is a biomarker of cartilage injury and plays a functional role in chondrocyte apoptosis

Ren, Guomin; Whittaker, Jackie L.; Léonard, Catherine; Rantere, D. De; Pang, Daniel S. J.; Salo, Paul; Fritzler, Marvin J.; Kapoor, Mohit; Koning, A. P. Jason de; Jaremko, J.L.; Emery, Carolyn A.; Krawetz, Roman

doi:10.1016/j.cyto.2018.11.030

Cited by 13 publications

(12 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Its role in inflammation could be considered quite ambiguous, since this potent chemotactic molecule affects both anti- and pro-inflammatory leukocytes [ 33 ]. It was also implied that CCL22, through pro-apoptotic activity on chondrocytes, takes direct part in initiating cartilage degeneration in OA—chemokine was appointed biomarker of cartilage degeneration in OA [ 34 ] and potential biomarker of early OA [ 35 ]. Surprisingly, CCL22 serum levels were lowered in our RA patients when compared to OA volunteers, but the differences in protein concentrations in synovial fluid samples did not reach statistical significance.…”

Section: Discussionmentioning

confidence: 99%

“…To the best of our knowledge, there are no publications concerning CCL22 levels in hypertensive patients, but murine model analyses performed by Zhong et al suggest increased chemokine secretion due to disease development [ 38 ]. Ren et al described increased protein expression in articular chondrocytes during OA-induced cartilage damage [ 34 ]. The following studies of this group also revealed: heightened synovial fluid chemokine concentration in OA group when compared to healthy subjects, its correlation with synovitis and constricting impact of CCL22 on anti-inflammatory cytokines expression ( 33 ).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Cytokines and chemokines multiplex analysis in patients with low disease activity rheumatoid arthritis

et al. 2022

View full text Add to dashboard Cite

Rheumatoid arthritis is a severe chronic autoimmune disorder that results from pathological activation of immune cells and altered cytokine/chemokine network. The aim of our study was to evaluate concentrations of chosen cytokines and chemokines in blood sera and synovial fluid samples isolated from low disease activity rheumatoid arthritis (RA) patients and osteoarthritis (OA) sufferers. Blood sera and synovial fluid samples have been obtained from 24 OA and 14 RA patients. Cytokines/chemokines levels have been determined using a Milliplex® Map 38-plex human cytokine/chemokine magnetic bead-based panel (Merck Millipore, Germany) and Luminex® MAGPIX® platform (Luminex USA). Low disease activity RA patients showed altered concentration of numerous cytokine/chemokine when compared to OA controls—they were characterized by, inter alia, increased: eotaxin/CCL11 (p = 0.037), GRO/CXCL1 (p = 0.037), IL-2 (p = 0.013), IL-4 (p = 0.017), IL-7 (p = 0.003), IL-8 (p = 0.0007) and GM-CSF (p = 0.037) serum levels, whilst MDC/CCL22 concentration was decreased in this group (p = 0.034). Eotaxin/CCL11 (p = 0.001), GRO/CXCL1 (p = 0.041), IL-10 (p = 0.003), GM-CSF (p = 0.01), IL-1RA (p = 0.0005) and VEGF (p = 0.01) concentrations in synovial fluid of RA females were also increased. Even with low disease activity score, RA patients exhibited increased concentrations of cytokines with pro- and anti-inflammatory activities, as well as numerous chemokines, growth factors and regulators of angiogenesis. Surprisingly, RA subjects also shown decreased concentration of CCL22 chemokine. The attempt to restore cytokine balance and tolerogenic environment is ineffective in RA sufferers even with good disease management. Distinguished factors could serve as possible indicators of disease progression even in low disease activity patients.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Cytokines and chemokines multiplex analysis in patients with low disease activity rheumatoid arthritis

et al. 2022

View full text Add to dashboard Cite

show abstract

“…Standardized joint injuries ( n = 5) were created while each rat was anesthetized using isoflurane delivered in oxygen [ 57 , 58 ]. A medial para-patellar arthrotomy was performed under a dissection microscope.…”

Section: Methodsmentioning

confidence: 99%

Synovial mesenchymal progenitor derived aggrecan regulates cartilage homeostasis and endogenous repair capacity

Krawetz

Bertram

et al. 2022

Cell Death Dis

Self Cite

View full text Add to dashboard Cite

Aggrecan is a critical component of the extracellular matrix of all cartilages. One of the early hallmarks of osteoarthritis (OA) is the loss of aggrecan from articular cartilage followed by degeneration of the tissue. Mesenchymal progenitor cell (MPC) populations in joints, including those in the synovium, have been hypothesized to play a role in the maintenance and/or repair of cartilage, however, the mechanism by which this may occur is unknown. In the current study, we have uncovered that aggrecan is secreted by synovial MPCs from healthy joints yet accumulates inside synovial MPCs within OA joints. Using human synovial biopsies and a rat model of OA, we established that this observation in aggrecan metabolism also occurs in vivo. Moreover, the loss of the “anti-proteinase” molecule alpha-2 macroglobulin (A2M) inhibits aggrecan secretion in OA synovial MPCs, whereas overexpressing A2M rescues the normal secretion of aggrecan. Using mice models of OA and cartilage repair, we have demonstrated that intra-articular injection of aggrecan into OA joints inhibits cartilage degeneration and stimulates cartilage repair respectively. Furthermore, when synovial MPCs overexpressing aggrecan were transplanted into injured joints, increased cartilage regeneration was observed vs. wild-type MPCs or MPCs with diminished aggrecan expression. Overall, these results suggest that aggrecan secreted from joint-associated MPCs may play a role in tissue homeostasis and repair of synovial joints.

show abstract

“…A cartilage injury model was established in the intervention and model groups. 21 The specific protocol was as follows. The right hind limbs were prepared under aseptic conditions.…”

Section: Methodsmentioning

confidence: 99%

Expression and related mechanisms of miR-330-3p and S100B in an animal model of cartilage injury

Liang²

2021

J Int Med Res

View full text Add to dashboard Cite

Objective To investigate the roles of and relationship between microRNA (miR)-330-3p and S100 calcium-binding protein B (S100B) in an animal model of cartilage injury. Methods This study included 30 New Zealand male rabbits randomly divided into three groups: an intervention group, a model group and a sham surgery control group. Modelling was performed in the intervention and model groups, but in the sham surgery group, only the skin was cut. After modelling, the intervention and model groups were injected with the miR-330-3p overexpression vector GV268-miR-330-3p or the control GV268-N-ODN vector, respectively, twice a week for 7 weeks. Results Levels of interleukin-1β and tumour necrosis factor-α in the synovial fluid were significantly higher in the model group than in the intervention and control groups. The level of miR-330-3p in the cartilage tissue was significantly higher in the control group than in the model group but it was significantly lower compared with the intervention group. Levels of S100B, fibroblast growth factor receptor 1 and fibroblast growth factor-2 in the cartilage tissue of rabbits in the model group were significantly higher compared with the control and intervention groups. Conclusion These findings demonstrate that the upregulation of miR-330-3p can inhibit the expression of S100B.

show abstract

CCL22 is a biomarker of cartilage injury and plays a functional role in chondrocyte apoptosis

Cited by 13 publications

References 51 publications

Cytokines and chemokines multiplex analysis in patients with low disease activity rheumatoid arthritis

Cytokines and chemokines multiplex analysis in patients with low disease activity rheumatoid arthritis

Synovial mesenchymal progenitor derived aggrecan regulates cartilage homeostasis and endogenous repair capacity

Expression and related mechanisms of miR-330-3p and S100B in an animal model of cartilage injury

Contact Info

Product

Resources

About