“In vitro” studies on galectin-3 in human natural killer cells

Brittoli, Alvaro; Fallarini, Silvia; Zhang, Hao; Pieters, Roland J.; Lombardi, Grazia

doi:10.1016/j.imlet.2017.12.004

Cited by 18 publications

(13 citation statements)

References 60 publications

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“…Gal-3 is known to regulate immune responses, acting as a pro-inflammatory signal with diverse innate immune cell targets to promote their activation, degranulation, and cytokine production 29,30 . In this context, recent in vitro studies have shown that endogenous expression of gal-3 in human NK cells can be stimulated by activating cytokines (IL-2, IL-15) and correlates functionally with their degree of cytotoxic degranulation 31 . While similar functions remain to be examined in the context of pregnancy, the identification of an endogenous gal-3 ligand localizing specifically to mouse uNK perforin granules 32 implies a potential role of this lectin in controlling the activation status of this particular lymphocyte subset, which has been ascribed important roles in the modulation of decidual development, trophoblast invasion, and maternal vascular remodeling during early pregnancy.…”

Section: Discussionmentioning

confidence: 99%

Galectin-3 deficiency in pregnancy increases the risk of fetal growth restriction (FGR) via placental insufficiency

et al. 2020

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Fetal growth restriction (FGR) is the most common pregnancy complication in developed countries. Pregnancies affected by FGR, frequently concur with complications and high risk of neonatal morbidity and mortality. To date, no approved treatment is available for pregnant women affected with FGR. The objective of this study was to investigate the contribution of galectin-3 (gal-3), a β-galactoside binding protein involved in pregnancy, placental function and fetal growth. We demonstrated that lack of gal-3 during mouse pregnancy leads to placental dysfunction and drives FGR in the absence of a maternal preeclampsia syndrome. Analysis of gal-3 deficient dams revealed placental inflammation and malperfusion, as well as uterine natural killer cell infiltration with aberrant activation. Our results also show that FGR is associated with a failure to increase maternal circulating gal-3 levels during the second and third trimester in human pregnancies. Placentas from human pregnancies affected by FGR displayed lower gal-3 expression, which correlated with placental dysfunction. These data highlight the importance of gal-3 in the promotion of proper placental function, as its absence leads to placental disease and subsequent FGR.

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Section: Discussionmentioning

confidence: 99%

Galectin-3 deficiency in pregnancy increases the risk of fetal growth restriction (FGR) via placental insufficiency

et al. 2020

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“…Galectins are a family of beta-galactoside-binding proteins implicated in modulating cell-cell and cell-matrix interactions. LG3BP promotes integrin-mediated cell adhesion and influences different processes of immune response, such as NK cell activation and lymphokine-activated killer (LAK) cell cytotoxicity (64). PTX3 is involved in the regulation of innate resistance to pathogens and inflammatory reactions.…”

Section: Discussionmentioning

confidence: 99%

Extracellular Vesicles Mediate Mesenchymal Stromal Cell-Dependent Regulation of B Cell PI3K-AKT Signaling Pathway and Actin Cytoskeleton

et al. 2019

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Mesenchymal stromal cells (MSCs) are adult, multipotent cells of mesodermal origin representing the progenitors of all stromal tissues. MSCs possess significant and broad immunomodulatory functions affecting both adaptive and innate immune responses once MSCs are primed by the inflammatory microenvironment. Recently, the role of extracellular vesicles (EVs) in mediating the therapeutic effects of MSCs has been recognized. Nevertheless, the molecular mechanisms responsible for the immunomodulatory properties of MSC-derived EVs (MSC-EVs) are still poorly characterized. Therefore, we carried out a molecular characterization of MSC-EV content by high-throughput approaches. We analyzed miRNA and protein expression profile in cellular and vesicular compartments both in normal and inflammatory conditions. We found several proteins and miRNAs involved in immunological processes, such as MOES, LG3BP, PTX3, and S10A6 proteins, miR-155-5p, and miR-497-5p. Different in silico approaches were also performed to correlate miRNA and protein expression profile and then to evaluate the putative molecules or pathways involved in immunoregulatory properties mediated by MSC-EVs. PI3K-AKT signaling pathway and the regulation of actin cytoskeleton were identified and functionally validated in vitro as key mediators of MSC/B cell communication mediated by MSC-EVs. In conclusion, we identified different molecules and pathways responsible for immunoregulatory properties mediated by MSC-EVs, thus identifying novel therapeutic targets as safer and more useful alternatives to cell or EV-based therapeutic approaches.

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“…The up-regulation of these two proteins then could be disease specific and could participate in different neurodegenerative syndromes depending on the regional overexpression. LGALS3 is a beta-galactosidase binding protein expressed by almost all cell type, involved in several physiological functions like immune activation and apoptosis [49,50,51]. LGALS3 has been reported to show altered patterns of expression in different neurodegenerative diseases like Alzheimer disease (AD), Parkinson’s disease (PD) and ALS [34,52].…”

Section: Discussionmentioning

confidence: 99%

Neuroanatomical Quantitative Proteomics Reveals Common Pathogenic Biological Routes between Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Dementia (FTD)

Iridoy

Zubiri

Zelaya

et al. 2018

IJMS

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(1) Background: Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are neurodegenerative disorders with an overlap in clinical presentation and neuropathology. Common and differential mechanisms leading to protein expression changes and neurodegeneration in ALS and FTD were studied trough a deep neuroproteome mapping of the spinal cord. (2) Methods: A liquid chromatography tandem mass spectrometry (LC-MS/MS) analysis of the spinal cord from ALS-TAR DNA-binding protein 43 (TDP-43) subjects, ubiquitin-positive frontotemporal lobar degeneration (FTLD-U) subjects and controls without neurodegenerative disease was performed. (3) Results: 281 differentially expressed proteins were detected among ALS versus controls, while 52 proteins were dysregulated among FTLD-U versus controls. Thirty-three differential proteins were shared between both syndromes. The resulting data was subjected to network-driven proteomics analysis, revealing mitochondrial dysfunction and metabolic impairment, both for ALS and FTLD-U that could be validated through the confirmation of expression levels changes of the Prohibitin (PHB) complex. (4) Conclusions: ALS-TDP-43 and FTLD-U share molecular and functional alterations, although part of the proteostatic impairment is region- and disease-specific. We have confirmed the involvement of specific proteins previously associated with ALS (Galectin 2 (LGALS3), Transthyretin (TTR), Protein S100-A6 (S100A6), and Protein S100-A11 (S100A11)) and have shown the involvement of proteins not previously described in the ALS context (Methanethiol oxidase (SELENBP1), Peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (PIN-1), Calcyclin-binding protein (CACYBP) and Rho-associated protein kinase 2 (ROCK2)).

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“In vitro” studies on galectin-3 in human natural killer cells

Cited by 18 publications

References 60 publications

Galectin-3 deficiency in pregnancy increases the risk of fetal growth restriction (FGR) via placental insufficiency

Galectin-3 deficiency in pregnancy increases the risk of fetal growth restriction (FGR) via placental insufficiency

Extracellular Vesicles Mediate Mesenchymal Stromal Cell-Dependent Regulation of B Cell PI3K-AKT Signaling Pathway and Actin Cytoskeleton

Neuroanatomical Quantitative Proteomics Reveals Common Pathogenic Biological Routes between Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Dementia (FTD)

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