Galectin 3 and its binding protein in rheumatoid arthritis

Ohshima, Shiro; Kuchen, Stefan; Seemayer, Christian A.; Kyburz, Diego; Hirt, Astrid; Klinzing, Stephanie; Michel, Beat A.; Liu, Fu‐Tong; Neidhart, Michel

doi:10.1002/art.11287

Cited by 182 publications

(194 citation statements)

References 78 publications

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“…This result is consistent with clinical studies in patients with RA and juvenile idiopathic arthritis. 11,12 Furthermore, we demonstrated reduced T-cell infiltration and decreased angiogenesis in the synovial tissues of arthritic rats that received gene therapy. Consistently, the lymph node cells from rats treated with Lt.shGal3 or Lt.Gal1 had increased susceptibility to antigen-induced T-cell death.…”

Section: Discussionmentioning

confidence: 85%

“…10 In RA, the galectin-3-binding protein was particularly expressed at sites of bone destruction and, in contrast, the expression of galectin-1 was never found at sites of joint invasion. 11 Furthermore, defective mononuclear cell apoptosis in infiltrates of synovial tissues from juvenile RA correlated with upregulation of galectin-3 and downregulation of galectin-1. 12 In addition, not only being involved in inflammation, galectin-3 was reported to contribute to the activation of RA synovial fibroblasts.…”

Section: Introductionmentioning

confidence: 96%

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Intra-articular lentivirus-mediated delivery of galectin-3 shRNA and galectin-1 gene ameliorates collagen-induced arthritis

et al. 2010

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Different members of the galectin family may have inhibitory or stimulatory roles in controlling immune responses and regulating inflammatory reactions in autoimmune diseases such as rheumatoid arthritis (RA). A hypothetical model of a cross talk between galectin-1 and galectin-3 has been established in the circumstance of rheumatoid joints. As galectin-3 is a positive regulator and galectin-1 is a negative regulator of inflammation and autoimmune responses, in this study we evaluated the effects of local knockdown of galectin-3 or overexpression of galectin-1 on ameliorating collagen-induced arthritis (CIA) in rats. Lentiviral vectors encoding galectin-3 small hairpin RNA (shRNA) and galectin-1, as well as two control vectors expressing luciferase shRNA and green fluorescent protein, were individually injected intra-articularly into the ankle joints of rats with CIA, and their treatment responses were monitored by measuring the clinical, radiological and histological changes. Our results show that both knockdown of galectin-3 and overexpression of galectin-1 induced higher percentages of antigen-induced T-cell death in the lymph node cells from arthritic rats. Furthermore, these treatments significantly reduced articular index scores, radiographic scores and histological scores, accompanied with decreased T-cell infiltrates and reduced microvessel density in the ankle joints. Our findings implicate galectin-3 and galectin-1 as potential therapeutic targets for the treatment of RA.

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Section: Discussionmentioning

confidence: 85%

Section: Introductionmentioning

confidence: 96%

Intra-articular lentivirus-mediated delivery of galectin-3 shRNA and galectin-1 gene ameliorates collagen-induced arthritis

et al. 2010

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“…In tissue specimens of these patients, Galectin-1 is mostly detected at the synovial sublining layer and downregulated in the synovial fluid (7,(19)(20)(21)(22). Presence of specific autoantibodies, a common phenomenon for galectins in autoimmune diseases (23), may account for this decrease.…”

mentioning

confidence: 99%

Galectin-1 Couples Glycobiology to Inflammation in Osteoarthritis through the Activation of an NF-κB–Regulated Gene Network

Toegel

Weinmann

André

et al. 2016

The Journal of Immunology

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Osteoarthritis is a degenerative joint disease that ranks among the leading causes of adult disability. Mechanisms underlying osteoarthritis pathogenesis are not yet fully elucidated, putting limits to current disease management and treatment. Based on the phenomenological evidence for dysregulation within the glycome of chondrocytes and the network of a family of adhesion/growth-regulatory lectins, that is, galectins, we tested the hypothesis that Galectin-1 is relevant for causing degeneration. Immunohistochemical analysis substantiated that Galectin-1 upregulation is associated with osteoarthritic cartilage and subchondral bone histopathology and severity of degeneration (p < 0.0001, n = 29 patients). In vitro, the lectin was secreted and it bound to osteoarthritic chondrocytes inhibitable by cognate sugar. Glycan-dependent Galectin-1 binding induced a set of disease markers, including matrix metalloproteinases and activated NF-κB, hereby switching on an inflammatory gene signature (p < 10−16). Inhibition of distinct components of the NF-κB pathway using dedicated inhibitors led to dose-dependent impairment of Galectin-1–mediated transcriptional activation. Enhanced secretion of effectors of degeneration such as three matrix metalloproteinases underscores the data’s pathophysiological relevance. This study thus identifies Galectin-1 as a master regulator of clinically relevant inflammatory-response genes, working via NF-κB. Because inflammation is critical to cartilage degeneration in osteoarthritis, this report reveals an intimate relation of glycobiology to osteoarthritic cartilage degeneration.

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“…Galectin-3 is reported to be involved in inflammation (Koca et al, 2014;Nielsen et al, 2014;Ohshima et al, 2003;Piper et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

“…Increased circulating levels of galectin-3 are associated with inflammatory severity in some inflammatory diseases, for example, systemic lupus erythematosus, rheumatoid arthritis, heart failure, and systemic sclerosis (Koca et al, 2014;Nielsen et al, 2014;Ohshima et al, 2003;Piper, de Courcey, Sherwood, Amin-Youssef, & McDonagh, 2016). Of note, activated glia can express galectin-3 during neuroinflammation (Boza-Serrano et al, 2014;Chen, Liao, Lin, & Liu, 2014;Sirko et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Serum galectin‐3 levels and delirium among postpartum intensive care unit women

Zhu

et al. 2017

Brain and Behavior

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Objective: Inflammation correlates with delirium. Galectin-3 is a proinflammatory protein. This study aimed to determine relation of serum galectin-3 levels to delirium of postpartum intensive care unit (ICU) women. Materials and Methods:In this prospective observational study, serum galectin-3, S100B, and C-reactive protein levels of 412 postpartum ICU women and 412 healthy women were measured. Delirium and Acute Physiology and Chronic Health Care Evaluation II (APCHCE II) scores were recorded.Results: Serum levels of galectin-3, S100B, and C-reactive protein were significantly elevated in the postpartum women than in the healthy women. Galectin-3 levels were highly associated with APCHCE II scores and S100B and C-reactive protein levels.Galectin-3, C-reactive protein, and S100B levels and APCHCE II scores were identified as independent predictors for delirium. Area under the curve (AUC) of serum galectin-3 levels was similar to that of S100B levels, and significantly exceeded those of Creactive protein levels and APCHCE II scores. Moreover, galectin-3 significantly improved the AUCs of APCHCE II scores, S100B levels, and C-reactive protein levels. Conclusions:Galectin-3, involved in inflammatory process underlying delirium-related brain injury, might be a potential biomarker to predict delirium of postpartum ICU women. K E Y W O R D Sdelirium, galectin-3, intensive care unit, postpartum, women

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Galectin 3 and its binding protein in rheumatoid arthritis

Cited by 182 publications

References 78 publications

Intra-articular lentivirus-mediated delivery of galectin-3 shRNA and galectin-1 gene ameliorates collagen-induced arthritis

Intra-articular lentivirus-mediated delivery of galectin-3 shRNA and galectin-1 gene ameliorates collagen-induced arthritis

Galectin-1 Couples Glycobiology to Inflammation in Osteoarthritis through the Activation of an NF-κB–Regulated Gene Network

Serum galectin‐3 levels and delirium among postpartum intensive care unit women

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