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Retinal caveolin-1 modulates neuroprotective signaling.
Adv. Exp. Med. Biol. 854, 411-418 (2016)
Caveolin-1 (Cav-1), the scaffolding protein of caveolae, is expressed in several retinal cell types and is associated with ocular pathologies. Cav-1 modulates neuroinflammatory/neuroprotective responses to central nervous system injury. We have shown that loss of Cav-1 results in a blunted cytokine response in retinas challenged with inflammatory stimuli. As neuroinflammatory and neuroprotective signaling overlap in their cytokine production and downstream signaling pathways, we hypothesized that loss of Cav-1 may also suppress neuroprotective signaling in the retina. To test this, we subjected mice in which Cav-1 was deleted specifically in the retina to a neurodegenerative insult induced by sodium iodate (NaIO3) and measured STAT3 activation, a measure of neuroprotective signaling. Our results show that Cav-1 ablation blunts STAT3 activation induced by NaIO3. STAT3 activation in response to intravitreal administration of the IL-6 family cytokine, leukemia inhibitory factor (LIF), was not affected by Cav-1 deletion indicating a competent gp130 receptor response. Thus, Cav-1 modulates neuroprotective signaling by regulating the endogenous production of neuroprotective factors.
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Publication type
Article: Journal article
Document type
Scientific Article
Editors
Bowes Rickman, C.* ; LaVail, M.M.* ; Anderson, R.E.* ; Grimm, C.* ; Hollyfield, J.G.* ; Ash, J.*
Keywords
Caveolin-1 ; Cre/lox ; Conditional Knockout ; Neuroprotection ; Cytokines ; Sodium Iodate ; Stat3; Breakdown; Barrier
ISSN (print) / ISBN
0065-2598
Conference Title
Retinal Degenerative Diseases : Mechanisms and Experimental Therapy
Quellenangaben
Volume: 854,
Pages: 411-418
Publisher
Springer
Publishing Place
New York
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
CF Metabolomics & Proteomics (CF-MPC)