Resistin is elevated following traumatic joint injury and causes matrix degradation and release of inflammatory cytokines from articular cartilage in vitro

Lee, J.H.; Ort, Tatiana; Ma, Kai; Picha, Kathleen S.; Carton, Jill M.; Marsters, P; Lohmander, L. Stefan; Baribaud, Frédéric; Song, Xiaoyu; Blake, S

doi:10.1016/j.joca.2008.08.007

Cited by 107 publications

(93 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Resistin can be detected locally in the synovium of inflamed joints in both rheumatoid arthritis (RA) and OA (Senolt et al 2007;Koskinen et al 2014). Furthermore, resistin increased expression of MMP-1, MMP-13, and ADAMTS-4 in human articular chondrocytes and stimulates proteoglycan degradation, as well as inhibited the production of proteoglycan and type II collagen in mouse and human cartilage explants (Lee et al 2009;Poonpet and Honsawek 2014). In addition, resistin can stimulate inflammatory cytokines, such as IL-6 and TNF-α, as well as PGE 2 synthesis.…”

Section: Discussionmentioning

confidence: 94%

Circulating levels of adiponectin, resistin, and visfatin after mud-bath therapy in patients with bilateral knee osteoarthritis

et al. 2015

View full text Add to dashboard Cite

Adipocytokines, including adiponectin, resistin, and visfatin may play an important role in the pathophysiology of osteoarthritis (OA). Spa therapy is one of the most commonly used non-pharmacological approaches for OA, but its mechanisms of action are not completely known. The aim of the present study was to assess whether a cycle of mud-bath therapy (MBT) influences the serum levels of adiponectin, resistin, and visfatin in patients with knee OA. As part of a prospective randomized, single blind-controlled trial evaluating the efficacy of MBT in knee OA, we included in this study 95 outpatients. One group (n = 49) received a cycle of MBT at the spa center of Chianciano Terme (Italy) in addition to the usual treatment, and one group (control group; n = 46) continued their regular care routine alone. Patients were assessed at basal time and at the end of the study (15 days) for clinical and biochemical parameters. Clinical assessments included spontaneous pain on a visual analog scale (VAS) score and the Western Ontario and McMaster Universities index (WOMAC) subscores for knee OA evaluated as total pain score (W-TPS), total stiffness score (W-TSS), and total physical function score (W-TPFS). Adiponectin, resistin and visfatin serum levels were assessed by enzyme immunoassay methods. At the end of the mud-bath therapy, serum adiponectin levels showed a significant decrease (p < 0.001), while no significant modifications were found in the control group at day 15. Serum resistin showed a significant decrease (p < 0.0001) in the MBT group at the end of the study and a significant increase in the control patients (p < 0.001). No significant modifications of visfatin were found in MBT. Furthermore, we tested the relationships between demographic and clinical parameters and adipocytokine concentrations measured in the MBT group at basal and at the end of the study. In conclusion, the present study shows that a cycle of MBT can modify serum levels of adiponectin and resistin but not the circulating levels of visfatin. In view of the recent evidences about the involvement of adiponectin and resistin in the pathogenesis and progression of OA, the decrease of these adipokines after mud-bath therapy may play a protective role in the course of the disease. However, it remains to be clarified which of the mechanisms of action of MBT may have determined the changes in serum levels of adiponectin and resistin that we observed.

show abstract

Section: Discussionmentioning

confidence: 94%

Circulating levels of adiponectin, resistin, and visfatin after mud-bath therapy in patients with bilateral knee osteoarthritis

et al. 2015

View full text Add to dashboard Cite

show abstract

“…Gonzales-Gay et al [35] observed decreased serum resistin level in patients with rheumatoid arthritis after anti-TNF-a therapy. Kaser et al and Lee et al [11,36] found that resistin was elevated both systemically and locally immediately following joint injury and has a direct effect on proinflammatory cytokine production. They suggest that resistin may play a role as an early marker of trauma-induced osteoarthritis.…”

Section: Discussionmentioning

confidence: 98%

Usefulness of Assessing Circulating Levels of Resistin, Ghrelin, and IL-18 in Alcoholic Acute Pancreatitis

et al. 2010

View full text Add to dashboard Cite

show abstract

“…It can be expected that this increase in a wide range of chemokines will have a significant impact on the cells of cartilage and other related joint tissues and should be considered in the pathophysiology of OA. Recently, we demonstrated that the adipokine, resistin, present in injured joints (12), also increased chemokine genes at both the transcriptional and post-transcriptional levels (13) in temporal patterns similar to the IL-1␤ patterns (6). The post-transcriptional regulation of chemokines was further investigated by us in chondrocytes with resistin (13) and by others in fibroblasts (14).…”

mentioning

confidence: 91%

CCAAT/Enhancer-binding Protein β and NF-κB Mediate High Level Expression of Chemokine Genes CCL3 and CCL4 by Human Chondrocytes in Response to IL-1β*

Zhang

Bryan²,

DeLassus³

et al. 2010

Journal of Biological Chemistry

View full text Add to dashboard Cite

Resistin is elevated following traumatic joint injury and causes matrix degradation and release of inflammatory cytokines from articular cartilage in vitro

Cited by 107 publications

References 39 publications

Circulating levels of adiponectin, resistin, and visfatin after mud-bath therapy in patients with bilateral knee osteoarthritis

Circulating levels of adiponectin, resistin, and visfatin after mud-bath therapy in patients with bilateral knee osteoarthritis

Usefulness of Assessing Circulating Levels of Resistin, Ghrelin, and IL-18 in Alcoholic Acute Pancreatitis

CCAAT/Enhancer-binding Protein β and NF-κB Mediate High Level Expression of Chemokine Genes CCL3 and CCL4 by Human Chondrocytes in Response to IL-1β*

Contact Info

Product

Resources

About