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Alpha2-Adrenergic–Agonist Brimonidine Stimulates Negative Feedback and Attenuates Injury-Induced Phospho-ERK and Dedifferentiation of Chicken Müller Cells
Author(s) -
Mohammad HarunOrRashid,
Marta DiazdelCastillo,
Caridad GalindoRomero,
Finn Hallböök
Publication year - 2015
Publication title -
investigative ophthalmology and visual science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.935
H-Index - 218
eISSN - 1552-5783
pISSN - 0146-0404
DOI - 10.1167/iovs.15-16816
Subject(s) - mapk/erk pathway , microbiology and biotechnology , agonist , signal transduction , receptor , downregulation and upregulation , biology , endocrinology , chemistry , medicine , biochemistry , gene
Retinal injury induces Müller cell dedifferentiation by activating extracellular signal-regulated kinase (ERK) signaling. Stimulation of α2-adrenergic receptors protects against injury but also activates ERK in Müller cells. The purpose of this work was to study the effect of α2-adrenergic signaling on injury-induced ERK and Müller cell dedifferentiation. We tested the hypothesis that α2-stimulation triggers negative feedback regulation of the injury-induced ERK pathway that attenuates Müller cell dedifferentiation.

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