Retinal caveolin-1 modulates neuroprotective signaling

Alaina Reagan, Xiaowu Gu, Stefanie M. Hauck, John D. Ash, Guangwen Cao, Timothy C. Thompson, Michael H. Elliott

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

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.

Original languageEnglish (US)
Title of host publicationAdvances in Experimental Medicine and Biology
PublisherSpringer New York LLC
Pages411-418
Number of pages8
DOIs
StatePublished - Oct 1 2016
Externally publishedYes

Publication series

NameAdvances in Experimental Medicine and Biology
Volume854
ISSN (Print)0065-2598
ISSN (Electronic)2214-8019

Keywords

  • Caveolin-1
  • Conditional knockout
  • Cre/lox
  • Cytokines
  • Neuroprotection
  • Sodium Iodate
  • STAT3

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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