Enhanced Ccl2-Ccr2 signaling drives more severe choroidal neovascularization with aging.

Abstract:

:The impact of many inflammatory diseases is influenced by age-related changes in the activation of resident and circulating myeloid cells. In the eye, a major sight-threatening consequence of age-related macular degeneration is the development of severe choroidal neovascularization (CNV). To identify the molecular pathways and myeloid cell populations involved in this increased neovascular response, we characterized the immune status of murine choroid and retina during aging and in the context of experimental CNV. In the choroid, but not in the retina, advancing age is associated with proinflammatory upregulation of CCL2-CCR2 signaling. Genetic excision of CCL2 diminishes age-related inflammatory changes in the choroid, with reduced recruitment of proinflammatory myeloid cells and attenuation of CNV. These findings indicate that CCL2-driven recruitment of myeloid cells contributes to increased severity of CNV with age. Similar mechanisms may be involved in other age-related inflammatory diseases.

journal_name

Neurobiol Aging

journal_title

Neurobiology of aging

authors

Robbie SJ,Georgiadis A,Barker SE,Duran Y,Smith AJ,Ali RR,Luhmann UFO,Bainbridge JW

doi

10.1016/j.neurobiolaging.2015.12.019

subject

Has Abstract

pub_date

2016-04-01 00:00:00

pages

110-119

eissn

0197-4580

issn

1558-1497

pii

S0197-4580(15)00635-1

journal_volume

40

pub_type

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