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

16 Scopus citations


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
Number of pages8
StatePublished - Oct 1 2016
Externally publishedYes

Publication series

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


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

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)


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