Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 23, Issue 23, Pages -Publisher
MDPI
DOI: 10.3390/ijms232315319
Keywords
Galectin-3; skin; fibrosis
Funding
- Spanish Ministerio de Ciencia e Innovacion
- Agencia Estatal de Investigacion, Instituto de Salud Carlos III FIS
- CIBERES group
- Spanish Government
- Generalitat Valenciana
- [PID2020-114871RB-I00]
- [CB06/06/0027]
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This study investigates the role of GAL-3 in skin fibrosis and demonstrates its significantly increased expression using various models and techniques.
Skin 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 beta 1 (TGF beta 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.
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