Atorvastatin inhibits CXCR7 induction to reduce macrophage migration

Ma, Wanshu; Liu, Yiwei; Wang, Chuan; Zhang, Lingxin; Crocker, Laura; Shen, Jianzhong

doi:10.1016/j.bcp.2014.02.014

Cited by 27 publications

(23 citation statements)

References 32 publications

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“…Although statins are known for their pleiotropic effects, pravastatin did not have a clear modulatory effect on OA synovial tissue in our study. On polarized macrophages however, pravastatin increased sCD163 production in both anti-inflammatory phenotypes, which is in line with other studies that have shown antiinflammatory effects of statins on macrophage polarization 42,43 , chondrocytes 44,45 , and progression of OA and arthritis in vivo 46,47 . Additionally, systemic statin use has also been shown to be associated with reduced progression of knee OA 48 and seemed to reduce the activity of rheumatoid arthritis in humans 49 .…”

Section: Discussionsupporting

confidence: 91%

Guiding synovial inflammation by macrophage phenotype modulation: an in vitro study towards a therapy for osteoarthritis

Utomo

Osch

Bayon

et al. 2016

Osteoarthritis and Cartilage

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These data indicate that macrophage phenotype modulation can be used to guide joint inflammation and thereby contribute to the development of new therapies to delay the progression of OA. The varying effects of the compounds on synovium of different degrees of inflammation, indicate that the modulatory capacity of the compounds depends on OA stage and underlines the importance of identifying this stadium for adequate treatment.

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Section: Discussionsupporting

confidence: 91%

Guiding synovial inflammation by macrophage phenotype modulation: an in vitro study towards a therapy for osteoarthritis

Utomo

Osch

Bayon

et al. 2016

Osteoarthritis and Cartilage

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“…Interestingly, the level of C-X-C chemokine receptor type 7 (CXCR7), also known as atypical chemokine receptor 3 (ACKR3), was significantly increased in response to FGFR3 deficiency (figure 4G). Previous studies showed that upregulation of CXCR7 could promote cell chemotaxis25 and enhance the recruitment of macrophages into inflammatory tissues 26. Furthermore, CXCR7 was specifically upregulated in the age-dependent osteoarthritis 27.…”

Section: Resultsmentioning

confidence: 95%

“…Previous studies reported that CXCR7 could enhance CXCL12-dependent chemotaxis of macrophages 25 26. Therefore, we assessed the chemotaxis of bone marrow–derived macrophages (BMDMs) in the presence or absence of CXCL12 using transwell migration assays (figure 5A).…”

Section: Resultsmentioning

confidence: 99%

FGFR3 deficiency enhances CXCL12-dependent chemotaxis of macrophages via upregulating CXCR7 and aggravates joint destruction in mice

Kuang

et al. 2019

Ann Rheum Dis

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ObjectivesThis study aims to investigate the role and mechanism of FGFR3 in macrophages and their biological effects on the pathology of arthritis.MethodsMice with conditional knockout of FGFR3 in myeloid cells (R3cKO) were generated. Gait behaviours of the mice were monitored at different ages. Spontaneous synovial joint destruction was evaluated by digital radiographic imaging and μCT analysis; changes of articular cartilage and synovitis were determined by histological analysis. The recruitment of macrophages in the synovium was examined by immunostaining and monocyte trafficking assay. RNA-seq analysis, Western blotting and chemotaxis experiment were performed on control and FGFR3-deficient macrophages. The peripheral blood from non-osteoarthritis (OA) donors and patients with OA were analysed. Mice were treated with neutralising antibody against CXCR7 to investigate the role of CXCR7 in arthritis.ResultsR3cKO mice but not control mice developed spontaneous cartilage destruction in multiple synovial joints at the age of 13 months. Moreover, the synovitis and macrophage accumulation were observed in the joints of 9-month-old R3cKO mice when the articular cartilage was not grossly destructed. FGFR3 deficiency in myeloid cells also aggravated joint destruction in DMM mouse model. Mechanically, FGFR3 deficiency promoted macrophage chemotaxis partly through activation of NF-κB/CXCR7 pathway. Inhibition of CXCR7 could significantly reverse FGFR3-deficiency-enhanced macrophage chemotaxis and the arthritic phenotype in R3cKO mice.ConclusionsOur study identifies the role of FGFR3 in synovial macrophage recruitment and synovitis, which provides a new insight into the pathological mechanisms of inflammation-related arthritis.

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“…SDF-1 is one of the factors excreted by atherosclerotic plaques and can bind to its receptor CXCR4 which is expressed at various levels on subtypes of monocytes and macrophages [8][9][10][11]. The SDF-1/CXCR4 signaling may hence depict another crucial mechanism for monocyte and macrophage control of atherosclerotic processes.…”

Section: Introductionmentioning

confidence: 98%

DPP-4 inhibition ameliorates atherosclerosis by priming monocytes into M2 macrophages

Brenner

Franz

Kühlenthal³

et al. 2015

International Journal of Cardiology

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Atorvastatin inhibits CXCR7 induction to reduce macrophage migration

Cited by 27 publications

References 32 publications

Guiding synovial inflammation by macrophage phenotype modulation: an in vitro study towards a therapy for osteoarthritis

Guiding synovial inflammation by macrophage phenotype modulation: an in vitro study towards a therapy for osteoarthritis

FGFR3 deficiency enhances CXCL12-dependent chemotaxis of macrophages via upregulating CXCR7 and aggravates joint destruction in mice

DPP-4 inhibition ameliorates atherosclerosis by priming monocytes into M2 macrophages

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