The TGFβ/Notch axis facilitates Muller cell-to-epithelial transition to ultimately form a chronic glial scar.

ABSTRACT:

Background

Contrasting with zebrafish, retinal regeneration from Müller cells (MCs) is largely limited in mammals, where they undergo reactive gliosis that consist of a hypertrophic response and ultimately results in vision loss. Transforming growth factor β (TGFβ) is essential for wound healing, including both scar formation and regeneration. However, targeting TGFβ may affect other physiological mechanisms, owing its pleiotropic nature. The regulation of various cellular activities by TGFβ relies on its interaction with other pathways including Notch. Here, we explore the interplay of TGFβ with Notch and how this regulates MC response to injury in zebrafish and mice. Furthermore, we aimed to characterize potential similarities between murine and human MCs during chronic reactive

SUBMITTER: Conedera FM 

PROVIDER: S-EPMC8482586 | biostudies-literature | 2021 Sep

REPOSITORIES: biostudies-literature