Literature DB >> 25752496

Toll-like receptor-4 knockout mice are more resistant to optic nerve crush damage than wild-type mice.

Dana Morzaev1,2, James D Nicholson1,2, Tomm Caspi2, Shirel Weiss1,2, Edith Hochhauser2,3, Nitza Goldenberg-Cohen1,2,4.   

Abstract

BACKGROUND: This study aims to investigate the role of the inflammatory response following optic nerve crush (ONC) in knockout mice for the toll-like receptor-4 gene (TLR4-/-) compared to wild-type (WT) mice.
METHODS: ONC was induced in TLR4-/- and C57BL6 WT mice. Histological sections of the retina and optic nerve were analysed on days 1, 3 or 21 after injury. Molecular analysis with real-time quantitative polymerase chain reaction was used to study the expression of CD45, tumour necrosis-alpha (TNF-α) and glial fibrillary acidic protein, as well as retinal ganglion cell (RGC) markers THY-1 and Brn3b.
RESULTS: There was a 25.5% and 38% loss in the RGC layer of the ONC-injured eyes of the TLR4-/- and the WT mice, respectively (with 27% and 9% of the remaining cells positive for Brn3a, respectively). Mean levels of Thy-1 and Brn3b were higher in the TLR4-/- mice. CD45 and Iba1 staining revealed infiltration of inflammatory cells into the injured nerve and retina in both groups. Molecular analysis of the optic nerve on day 1 showed increased TNF-α expression and reduced CD45 and GFAP expression; on day 3, CD45 reverted to baseline but GFAP remained low; on day 21, all 3 markers were at baseline in the TLR4-/- group and decreased in the WT group.
CONCLUSION: Inflammation plays a major role in the response to ONC injury. Reduced levels of inflammation are associated with improved RGC preservation. The increase in TNF-α and reduction in CD45 in both TLR4-/- and WT mice may indicate the presence of an alternative pathway for induction of RGC death.
© 2015 Royal Australian and New Zealand College of Ophthalmologists.

Entities:  

Keywords:  TLR-4 knockout mouse; ischemic retina; neuroprotection; optic nerve crush model

Mesh:

Substances:

Year:  2015        PMID: 25752496     DOI: 10.1111/ceo.12521

Source DB:  PubMed          Journal:  Clin Exp Ophthalmol        ISSN: 1442-6404            Impact factor:   4.207


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