Analysis of Smad3 in the modulation of stromal extracellular matrix proteins in corneal scarring after alkali injury.
Rattachement africain : us. Niveau de preuve : code pays fourni par la source.
Le résumé fourni par la source
Purpose: deficient mice. Methods: /J) mouse strains. Slit-lamp and stereo microscopy were used for clinical assessment and corneal haze grading in live animals. Hematoxylin and eosin and Masson's trichrome staining were used to study comparative morphology and collagen level alterations between the groups. Real-time qRT-PCR, western blot, and immunohistochemistry were used to measure changes in profibrotic genes at the mRNA and protein levels. Results: deficient mice. Conclusions: The significant changes in profibrotic genes and stromal ECM proteins revealed a direct role of Smad3 in stromal ECM proteins and TGFβ/Smad-driven wound healing. Smad3 appears to be an attractive molecular target for limiting abnormal stroma wound healing to treat corneal fibrosis in vivo.
Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.
Le contrôle bibliographique ouvert
Les institutions déclarées
Une affiliation ne permet pas de déduire la nationalité d’un auteur.