Synthesis and propagation of complement C3 by microglia/monocytes in the aging retina.

<h4>Introduction</h4>Complement activation is thought to contribute to the pathogenesis of age-related macular degeneration (AMD), which may be mediated in part by para-inflammatory processes. We aimed to investigate the expression and localization of C3, a crucial component of the compl...

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Autores principales:	Matt Rutar, Krisztina Valter, Riccardo Natoli, Jan M Provis
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2014
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/16db169d8f594c71b6f93963354ff8db
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spelling	oai:doaj.org-article:16db169d8f594c71b6f93963354ff8db2021-11-18T08:24:55ZSynthesis and propagation of complement C3 by microglia/monocytes in the aging retina.1932-620310.1371/journal.pone.0093343https://doaj.org/article/16db169d8f594c71b6f93963354ff8db2014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24705166/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Introduction</h4>Complement activation is thought to contribute to the pathogenesis of age-related macular degeneration (AMD), which may be mediated in part by para-inflammatory processes. We aimed to investigate the expression and localization of C3, a crucial component of the complement system, in the retina during the course of aging.<h4>Methods</h4>SD rats were born and reared in low-light conditions, and euthanized at post-natal (P) days 100, 450, or 750. Expression of C3, IBA1, and Ccl- and Cxcl- chemokines was assessed by qPCR, and in situ hybridization. Thickness of the ONL was assessed in retinal sections as a measure of photoreceptor loss, and counts were made of C3-expressing monocytes.<h4>Results</h4>C3 expression increased significantly at P750, and correlated with thinning of the ONL, at P750, and up-regulation of GFAP. In situ hybridization showed that C3 was expressed by microglia/monocytes, mainly from within the retinal vasculature, and occasionally the ONL. The number of C3-expressing microglia increased significantly by P750, and coincided spatiotemporally with thinning of the ONL, and up-regulation of Ccl- and Cxcl- chemokines.<h4>Conclusions</h4>Our data suggest that recruited microglia/monocytes contribute to activation of complement in the aging retina, through local expression of C3 mRNA. C3 expression coincides with age-related thinning of the ONL at P750, although it is unclear whether the C3-expressing monocytes are a cause or consequence. These findings provide evidence of activation of complement during natural aging, and may have relevance to cellular events underling the pathogenesis of age-related retinal diseases.Matt RutarKrisztina ValterRiccardo NatoliJan M ProvisPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 4, p e93343 (2014)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Matt Rutar Krisztina Valter Riccardo Natoli Jan M Provis Synthesis and propagation of complement C3 by microglia/monocytes in the aging retina.
description	<h4>Introduction</h4>Complement activation is thought to contribute to the pathogenesis of age-related macular degeneration (AMD), which may be mediated in part by para-inflammatory processes. We aimed to investigate the expression and localization of C3, a crucial component of the complement system, in the retina during the course of aging.<h4>Methods</h4>SD rats were born and reared in low-light conditions, and euthanized at post-natal (P) days 100, 450, or 750. Expression of C3, IBA1, and Ccl- and Cxcl- chemokines was assessed by qPCR, and in situ hybridization. Thickness of the ONL was assessed in retinal sections as a measure of photoreceptor loss, and counts were made of C3-expressing monocytes.<h4>Results</h4>C3 expression increased significantly at P750, and correlated with thinning of the ONL, at P750, and up-regulation of GFAP. In situ hybridization showed that C3 was expressed by microglia/monocytes, mainly from within the retinal vasculature, and occasionally the ONL. The number of C3-expressing microglia increased significantly by P750, and coincided spatiotemporally with thinning of the ONL, and up-regulation of Ccl- and Cxcl- chemokines.<h4>Conclusions</h4>Our data suggest that recruited microglia/monocytes contribute to activation of complement in the aging retina, through local expression of C3 mRNA. C3 expression coincides with age-related thinning of the ONL at P750, although it is unclear whether the C3-expressing monocytes are a cause or consequence. These findings provide evidence of activation of complement during natural aging, and may have relevance to cellular events underling the pathogenesis of age-related retinal diseases.
format	article
author	Matt Rutar Krisztina Valter Riccardo Natoli Jan M Provis
author_facet	Matt Rutar Krisztina Valter Riccardo Natoli Jan M Provis
author_sort	Matt Rutar
title	Synthesis and propagation of complement C3 by microglia/monocytes in the aging retina.
title_short	Synthesis and propagation of complement C3 by microglia/monocytes in the aging retina.
title_full	Synthesis and propagation of complement C3 by microglia/monocytes in the aging retina.
title_fullStr	Synthesis and propagation of complement C3 by microglia/monocytes in the aging retina.
title_full_unstemmed	Synthesis and propagation of complement C3 by microglia/monocytes in the aging retina.
title_sort	synthesis and propagation of complement c3 by microglia/monocytes in the aging retina.
publisher	Public Library of Science (PLoS)
publishDate	2014
url	https://doaj.org/article/16db169d8f594c71b6f93963354ff8db
work_keys_str_mv	AT mattrutar synthesisandpropagationofcomplementc3bymicrogliamonocytesintheagingretina AT krisztinavalter synthesisandpropagationofcomplementc3bymicrogliamonocytesintheagingretina AT riccardonatoli synthesisandpropagationofcomplementc3bymicrogliamonocytesintheagingretina AT janmprovis synthesisandpropagationofcomplementc3bymicrogliamonocytesintheagingretina
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Synthesis and propagation of complement C3 by microglia/monocytes in the aging retina.

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