| First Author | Lo YH | Year | 2021 |
| Journal | J Invest Dermatol | Volume | 141 |
| Issue | 3 | Pages | 503-511.e9 |
| PubMed ID | 32805218 | Mgi Jnum | J:304005 |
| Mgi Id | MGI:6510416 | Doi | 10.1016/j.jid.2020.07.021 |
| Citation | Lo YH, et al. (2021) Galectin-8 Is Upregulated in Keratinocytes by IL-17A and Promotes Proliferation by Regulating Mitosis in Psoriasis. J Invest Dermatol 141(3):503-511.e9 |
| abstractText | Psoriasis is a chronic inflammatory skin disease that develops under the influence of the IL-23/T helper 17 cell axis and is characterized by intense inflammation and prominent epidermal hyperplasia. In this study, we demonstrate that galectin-8, a beta-galactosidebinding lectin, is upregulated in the epidermis of human psoriatic skin lesions as well as in a mouse model of psoriasis induced by intradermal IL-23 injections and in IL-17Atreated keratinocytes. We show that keratinocyte proliferation is less prominent in galectin-8knockout mice after intradermal IL-23 treatment than in wild-type mice. In addition, we show that galectin-8 levels in keratinocytes are positively correlated with the ability of the cells to proliferate and that transitioning from mitosis into G1 phase is delayed in galectin-8knockout HaCaT cells after cell-cycle synchronization and release. We demonstrate by immunofluorescence staining and immunoblotting the presence of galectin-8 within the mitotic apparatus. We reveal by coimmunoprecipitation and mass spectrometry analysis that alpha-tubulin interacts with galectin-8 during mitosis. Finally, we show that in the absence of galectin-8, pericentrin compactness is lessened and mitotic microtubule length is shortened, as demonstrated by immunofluorescence staining. We conclude that galectin-8 is upregulated in psoriasis and contributes to the hyperproliferation of keratinocytes by maintaining centrosome integrity during mitosis through interacting with alpha-tubulin. |
