Evidence of a role for galectin-1 in acute inflammation

Rabinovich, Gabriel A.; Sotomayor, Claudia Elena; Riera, Clelia M.; Bianco, Ismael D.; Correa, Silvia G.

doi:10.1002/(sici)1521-4141(200005)30:5<1331::aid-immu1331>3.0.co;2-h

Cited by 162 publications

(131 citation statements)

References 46 publications

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“…7 Recently, it has been shown that administration of Gal-1 inhibited the acute inflammatory response in a mouse model of paw edema. 8 Interestingly, the latter study reported that Gal-1 anti-edema effect was associated with a reduced polymorphonuclear leukocyte (PMN) influx into the inflamed paws.…”

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confidence: 97%

A Novel Biological Activity for Galectin-1

Cao

Cerchiaro

et al. 2003

The American Journal of Pathology

134

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Galectin-1 (Gal-1), the prototype of a family of ␤-galactoside-binding proteins, has been shown to attenuate experimental acute and chronic inflammation. In view of the fact that endothelial cells (ECs), but not human polymorphonuclear leukocytes (PMNs), expressed Gal-1 we tested here the hypothesis that the protein could modulate leukocyte-EC interaction in inflammatory settings. In vitro, human recombinant (hr) Gal-1 inhibited PMN chemotaxis and trans-endothelial migration. These actions were specific as they were absent if Gal-1 was boiled or blocked by neutralizing antiserum. In vivo, hrGal-1 (optimum effect at 0.3 g equivalent to 20 pmol) inhibited interleukin-1␤-induced PMN recruitment into the mouse peritoneal cavity. Intravital microscopy analysis showed that leukocyte flux, but not their rolling velocity, was decreased by an anti-inflammatory dose of hrGal-1. Binding of biotinylated Gal-1 to resting and postadherent human PMNs occurred at concentrations inhibitory in the chemotaxis and transmigration assays. In addition , the pattern of Gal-1 binding was differentially modulated by PMN or EC activation.

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confidence: 97%

A Novel Biological Activity for Galectin-1

Cao

Cerchiaro

et al. 2003

The American Journal of Pathology

134

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“…Therefore, galectin-1 might have a protective role in RIF, partly through the inhibition of fibrotic cytokine TGF-β (8). Other recent studies have shown that galectin-1 suppresses the inflammatory response in collagen-induced arthritis via T-cell apoptosis (20) or inhibits both the soluble and cellular mediators of the inflammatory response (21), further supporting other protective roles of galectin-1.…”

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confidence: 70%

Overexpression of α1-protease Inhibitor and Galectin-1 in Radiation-induced Early Phase of Pulmonary Fibrosis

Kim

Song

et al. 2006

Cancer Res Treat

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Purpose: Radiation-induced pulmonary fibrosis (RIF) is a significant complication of radiotherapy for lung cancer. Despite the large number of studies, the molecular mechanisms of RIF are poorly understood. Therefore, the complex protein expression pattern in RIF was characterized by identifying the proteins with an altered expression level after thorax irradiation using two-dimensional electrophoresis (2-DE) and mass spectrometry.

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“…Roles for Gal-1 have been identified in such varied processes as embryogenesis, neurogenesis, hematopoiesis, T-cell homeostasis, and, notably, related to this study, in modulating acute inflammation (20). Gal-1 inhibits migration of neutrophils and mast cell degranulation in response to bee venom phospholipase A2 in vivo (21). Furthermore, the results of a study of eosinophils in nasal polyps suggested that the antiinflammatory actions of glucocorticoids might work in part through induction of Gal-1 (22).…”

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confidence: 70%