Inhibition of LPS-Induced Inflammatory Response of Oral Mesenchymal Stem Cells in the Presence of Galectin-3

Galectin-3 (GAL-3) is a beta-galactoside binding lectin produced by mesenchymal stem cells (MSCs) and other cell sources under inflammatory conditions. Several studies have reported that GAL-3 exerts an anti-inflammatory action, regulated by its natural ligand GAL-3 BP. In the present study, we aime...

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Bibliographic Details
Published in:Biomedicines 2023-05, Vol.11 (6), p.1519
Main Authors: Paganelli, Alessia, Diomede, Francesca, Marconi, Guya Diletta, Pizzicannella, Jacopo, Rajan, Thangavelu Soundara, Trubiani, Oriana, Paganelli, Roberto
Format: Article
Language:English
Subjects:
Bone marrow
Cell growth
Confocal microscopy
Cytokines
Ethylenediaminetetraacetic acid
Extracellular vesicles
GAL-3
galectin
Galectin-3
Immunofluorescence
Inflammation
ISO standards
Lectins
Lipopolysaccharides
LPS
Lymphocytes
mesenchymal stem cell
Mesenchymal stem cells
MyD88 protein
NF-κB protein
Pathogenesis
Stem cells
TLR
TLR4 protein
Toll-like receptors
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Summary:Galectin-3 (GAL-3) is a beta-galactoside binding lectin produced by mesenchymal stem cells (MSCs) and other cell sources under inflammatory conditions. Several studies have reported that GAL-3 exerts an anti-inflammatory action, regulated by its natural ligand GAL-3 BP. In the present study, we aimed to assess the GAL-3 mediated regulation of the MSC function in an LPS-induced inflammation setting. Human gingival mesenchymal stem cells (hGMSCs) were stimulated in vitro with LPSs; the expression of TLR4, NFκB p65, MyD88 and NALP3 were assessed in the hGMSCs via immunofluorescence imaging using confocal microscopy, Western blot assay, and RT-PCR before and after the addition of GAL-3, both alone and with the addition of its inhibitors. LPSs stimulated the expression of TLR4, NFκB p65, MyD88 and NALP3 in hGMSCs, which was inhibited by GAL-3. The addition of either GAL3-BP or the antibody to GAL-3 were able to revert the GAL-3-mediated effects, restoring the expression of TLR4, NFκB p65, MyD88 and NALP3. GAL-3 induces the downregulation of the LPS-induced inflammatory program in MSCs.
ISSN:2227-9059
2227-9059
DOI:10.3390/biomedicines11061519