期刊
BIOMEDICINES
卷 11, 期 6, 页码 -出版社
MDPI
DOI: 10.3390/biomedicines11061519
关键词
GAL-3; galectin; inflammation; LPS; mesenchymal stem cell; TLR; NF & kappa;B
Galectin-3 (GAL-3) inhibits the expression of TLR4, NF-κB p65, MyD88, and NALP3 in LPS-stimulated hGMSCs, and this inhibitory effect can be reversed by GAL-3 BP or GAL-3 antibody.
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, NF?B 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, NF?B 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, NF?B p65, MyD88 and NALP3. GAL-3 induces the downregulation of the LPS-induced inflammatory program in MSCs.
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