TNFα-Induced Disruption of the Blood–Retinal Barrier In Vitro Is Regulated by Intracellular 3′,5′-Cyclic Adenosine Monophosphate Levels | Zendy

AnneEva van der Wijk | Zendy; Ilse M. C. Vogels | Zendy; Cornelis J.F. Van Noorden | Zendy; Ingeborg Klaassen | Zendy; Reinier O. Schlingemann | Zendy

Open Access

TNFα-Induced Disruption of the Blood–Retinal Barrier In Vitro Is Regulated by Intracellular 3′,5′-Cyclic Adenosine Monophosphate Levels

Author(s) -

AnneEva van der Wijk,

Ilse M. C. Vogels,

Cornelis J.F. Van Noorden,

Ingeborg Klaassen,

Reinier O. Schlingemann

Publication year - 2017

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.16-21091

Subject(s) - blood–retinal barrier , tumor necrosis factor alpha , proinflammatory cytokine , barrier function , tight junction , cyclic adenosine monophosphate , chemistry , cyclic guanosine monophosphate , vascular permeability , microbiology and biotechnology , rhoa , biology , pharmacology , immunology , biochemistry , signal transduction , inflammation , endocrinology , nitric oxide , receptor , diabetes mellitus , diabetic retinopathy

Proinflammatory cytokines such as tumor necrosis factor (TNFα) may have a causative role in blood-retinal barrier (BRB) disruption, which is an essential step in the development of diabetic macular edema. The purpose of our study was to determine whether TNFα increases permeability in an in vitro model of the BRB and to explore the mechanisms involved.

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