Show simple item record

dc.contributor.authorRutar, M
dc.contributor.authorValter, K
dc.contributor.authorNatoli, R
dc.contributor.authorProvis, JM
dc.date.accessioned2021-02-12T00:27:25Z
dc.date.available2021-02-12T00:27:25Z
dc.date.issued2014-04-04
dc.identifierpii: PONE-D-13-34405
dc.identifier.citationRutar, M., Valter, K., Natoli, R. & Provis, J. M. (2014). Synthesis and Propagation of Complement C3 by Microglia/Monocytes in the Aging Retina. PLOS ONE, 9 (4), https://doi.org/10.1371/journal.pone.0093343.
dc.identifier.issn1932-6203
dc.identifier.urihttp://hdl.handle.net/11343/260610
dc.description.abstractINTRODUCTION: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
dc.languageEnglish
dc.publisherPUBLIC LIBRARY SCIENCE
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.titleSynthesis and Propagation of Complement C3 by Microglia/Monocytes in the Aging Retina
dc.typeJournal Article
dc.identifier.doi10.1371/journal.pone.0093343
melbourne.affiliation.departmentAnatomy and Neuroscience
melbourne.affiliation.facultyMedicine, Dentistry & Health Sciences
melbourne.source.titlePLoS One
melbourne.source.volume9
melbourne.source.issue4
dc.rights.licenseCC BY
melbourne.elementsid1110032
melbourne.contributor.authorRutar, Matthew
dc.identifier.eissn1932-6203
melbourne.accessrightsOpen Access


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record