Galectin-3: An open-ended story

Dumić, Jerka; Dabelić, Sanja; Flögel, Mirna

doi:10.1016/j.bbagen.2005.12.020

Cited by 1,013 publications

(1,101 citation statements)

References 216 publications

Supporting

Mentioning

1,017

Contrasting

Unclassified

Order By: Relevance

“…10 A number of intracellular functions have been reported for galectin-3, including positive growth regulatory ability on T cells. 24 While galectin-1 induces cell death, endogenous galectin-3 has anti-apoptotic function. 25 Recent studies suggest that endogenous galectin-3 brings about apoptosis resistance by engaging apoptosis regulation pathways or modulating homeostasis of mitochondria.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2010

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 99%

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

et al. 2010

View full text Add to dashboard Cite

show abstract

“…The alterations of the O-glycan structure of MUC1 that occurred in cancer cells, that is, presence of truncated chains such as Tn (GalNAca-) or TF (Galb1,3GalNA-ca-) antigen(s) (Hollingsworth and Swanson, 2004), can promote MUC1 endocytosis in a clathrin-dependent manner, and its intracellular sequestration (Altschuler et al, 2000). Interestingly, galectin-3, an endogenous lectin with one carbohydrate recognition domain showing binding specificity for b galactosides present in Nand O-linked glycans (Dumic et al, 2006) and encoded by LGALS3, was recently shown to interact directly with the N-glycoprotein EGFR (Partridge et al, 2004) or MUC1 (Yu et al, 2007). The latter requires the presence of unsialylated TF antigen on MUC1 and leads to a redistribution of MUC1 on the cell surface (Yu et al, 2007), exposure of adhesion molecules such as Ecadherin and increase of the survival of tumour cells (Zhao et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

“…Indeed, a previous report shows that galectin-3 regulated the apical delivery of glycoproteins through a raft-independent pathway in Madin-Darby canine kidney (MDCK) cells (Delacour et al, 2007). Galectin-3 is widely expressed in epithelial tissues mainly as a cytosolic protein but it can also be found in the nucleus, mitochondria or secreted outside the cell (Dumic et al, 2006). In the pancreas, galectin-3 is faintly expressed in normal ductal cells but strongly in most PDAC (Berberat et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Galectin-3 regulates MUC1 and EGFR cellular distribution and EGFR downstream pathways in pancreatic cancer cells

et al. 2011

View full text Add to dashboard Cite

MUC1 is a transmembrane glycoprotein which is typically expressed at the apical membrane of normal epithelial cells. In cancer cells, the over-expression of MUC1 and its aberrant localization around the cell membrane and in the cytoplasm favours its interaction with different protein partners such as epidermal growth factor receptor (EGFR) and can promote tumour proliferation through the activation of oncogenic signalling pathways. Our aims were to study the mechanisms inducing MUC1 cytoplasmic localization in pancreatic cancer cells, and to decipher their impact on EGFR cellular localization and activation. Our results showed that galectin-3, an endogenous lectin, is coexpressed with MUC1 in human pancreatic ductal adenocarcinoma, and that it favours the endocytosis of MUC1 and EGFR. Depletion of galectin-3 by RNA interference increased the interaction between MUC1 and EGFR, EGFR and ERK-1,2 phosphorylation, and translocation of EGFR to the nucleus. On the contrary, silencing of galectin-3 led to a decrease of cyclin-D1 levels and of cell proliferation. The galectin-3-dependent regulation of MUC1/EGFR functions may represent an interesting mechanism modulating the EGFR-stimulated cell growth of pancreatic cancer cells.

show abstract

“…Estudios previos han mostrado que los niveles plasmáticos de esta molécula tienen valor predictor de eventos cardiovasculares en pacientes con enfermedad coronaria 27,28 . Por otra parte, Gal-3 está involucrada en fenómenos de fibrosis y cáncer 13,29 . Nuestro grupo ha publicado con anterioridad que, en pacientes con enfermedad coronaria estable, MCP-1 tiene valor pronós-tico como predictor de eventos isquémicos agudos, mientras que NT-proBNP y Gal-3 predicen el desarrollo de IC y muerte 10 .…”

Section: Discussionunclassified

Impacto de los niveles plasmáticos de pro-péptido natriurético tipo B aminoterminal, proteína quimiotáctica de monocitos-1 y galectina3 en la capacidad predictiva de eventos de la escala clínica LIPID en la enfermedad coronaria estable

Higueras

Martı́n-Ventura

Blanco-Colio

et al. 2015

Clínica e Investigación en Arteriosclerosis

View full text Add to dashboard Cite

El acceso a la versión del editor puede requerir la suscripción del recurso Access to the published version may require subscriptionCómo citar este artículo: Higueras J, et al. Impacto de los niveles plasmáticos de pro-péptido natriurético tipo B aminoterminal, proteína quimiotáctica de monocitos-1 y galectina 3 en la capacidad predictiva de eventos de la escala clínica LIPID en la enfermedad coronaria estable. Objetivo: Analizar la utilidad pronóstica de la escala clínica de riesgo del estudio Long-Term Intervention with Pravastatin in Ischemic Disease (LIPID) y la mejora de su capacidad predictiva al combinarla con los niveles plasmáticos de MCP-1, galectina-3 y NT-proBNP en pacientes con ECE. Métodos y resultados:Se analizaron 706 pacientes con ECE y antecedentes de síndrome coronario agudo (SCA). Se realizó un seguimietno de 2,2 ± 0,99 años. El objetivo primario era la aparición de un evento isquémico (cualquier SCA, infarto cerebral o accidente isquémico transitorio), insuficiencia cardiaca o muerte. La escala clínica de riesgo predijo significativamente el desarrollo del objetivo primario, con un área bajo la curva receiver operating characteristic (ROC) de 0,642 (0,579-0,705); p < 0,001. Desarrollamos una escala combinada sumando a las puntuaciones de la escala LIPID los deciles de los niveles plasmáticos de MCP-1, galectina-3 y NT-proBNP. El nivel predictivo mejoró con un área bajo la curva de 0,744 (0,684-0,805); p < 0,001 (p = 0,022 para la comparación). Una puntuación > 21,5 mostró una sensibilidad del 74% y una especificidad del 61% para el desarrollo del objetivo primario (p < 0,001; test de log-rank). Conclusión: Los niveles plasmáticos de MCP-1, galectina-3 y NT-proBNP mejoran la capacidad de la escala clínica LIPID para predecir el pronóstico de los pacientes con ECE. © 2014 Sociedad Española de Arteriosclerosis. Publicado por Elsevier España, S.L.U. Todos los derechos reservados. KEYWORDSStable coronary artery disease; Galectine-3; NT-proBNP Impact of plasma pro-B-type natriuretic peptide amino-terminal and galectin-3 levels on the predictive capacity of the LIPID Clinical Risk Scale in stable coronary disease Abstract Introduction: At present, there is no tool validated by scientific societies for risk stratification of patients with stable coronary artery disease (SCAD). It has been shown that plasma levels of monocyte chemoattractant protein-1 (MCP-1), galectin-3 and pro-B-type natriuretic peptide amino-terminal (NT-proBNP) have prognostic value in this population. Objetive: To analyze the prognostic value of a clinical risk scale published in Long-term Intervention with Pravastatin in Ischemic Disease (LIPID) study and determining its predictive capacity when combined with plasma levels of MCP-1, galectin-3 and NT-proBNP in patients with SCAD. Methods and results: A total of 706 patients with SCAD and a history of acute coronary syndrome (ACS) were analyzed over a follow up period of 2.2 ± 0.99 years. The primary endpoint was the occurrence of an ischemic event (any SCA, stroke or transient ...

show abstract

Galectin-3: An open-ended story

Cited by 1,013 publications

References 216 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-3 regulates MUC1 and EGFR cellular distribution and EGFR downstream pathways in pancreatic cancer cells

Impacto de los niveles plasmáticos de pro-péptido natriurético tipo B aminoterminal, proteína quimiotáctica de monocitos-1 y galectina3 en la capacidad predictiva de eventos de la escala clínica LIPID en la enfermedad coronaria estable

Contact Info

Product

Resources

About