Peiró, TeresaAlonso Carpio, MiriamRibera, PilarAlmudéver, PatriciaRoger Laparra, InésMontero Magalló, PaulaMarín, SeverianoMilara, JavierCortijo, Julio2023-02-232023-02-232022Peiró, T., Alonso-Carpio, M., Ribera, P., Almudéver, P., Roger, I., Montero, P., Marín, S., Milara, J., & Cortijo, J. (2022). Increased expression of galectin-3 in skin fibrosis: Evidence from in vitro and in vivo studies. International Journal of Molecular Sciences, 23(23), 15319. https://doi.org/10.3390/ijms2323153191422-0067http://hdl.handle.net/11268/11829Skin fibrosis is a hallmark of a wide array of dermatological diseases which can greatly impact the patients’ quality of life. Galectin-3 (GAL-3) has emerged as a central regulator of tissue fibrosis, playing an important pro-fibrotic role in numerous organs. Various studies are highlighting its importance as a skin fibrotic diseases biomarker; however, there is a need for further studies that clarify its role. This paper aims to ascertain whether the expression of GAL-3 is increased in relevant in vitro and in vivo models of skin fibrosis. We studied the role of GAL-3 in vitro using normal human dermal fibroblasts (NHDF) and fibrocytes. In addition, we used a skin fibrosis murine model (BALB/c mice) and human biopsies of healthy or keloid tissue. GAL-3 expression was analyzed using real time PCR, Western blot and immunostaining techniques. We report a significantly increased expression of GAL-3 in NHDF and fibrocytes cell cultures following stimulation with transforming growth factor  1 (TGF 1). In vivo, GAL-3 expression was increased in a murine model of systemic sclerosis and in human keloid biopsies. In sum, this study underlines the involvement of GAL-3 in skin fibrosis using several models of the disease and highlights its role as a relevant target.engAtribución 4.0 Internacionalhttp://creativecommons.org/licenses/by/4.0/Galectina 3FibrosisCalidad de vidajournal article10.3390/ijms232315319open accessEnfermedad de la pielTratamiento médicoFarmacología