Back to Search Start Over

Imidazole Compounds for Protecting Choroidal Endothelial Cells from Complement Injury.

Authors :
Zeng S
Wen KK
Workalemahu G
Sohn EH
Wu M
Chirco KR
Flamme-Wiese MJ
Liu X
Stone EM
Tucker BA
Mullins RF
Source :
Scientific reports [Sci Rep] 2018 Sep 06; Vol. 8 (1), pp. 13387. Date of Electronic Publication: 2018 Sep 06.
Publication Year :
2018

Abstract

Age-related macular degeneration (AMD) is a common, blinding disease associated with increased complement system activity. Eyes with AMD show elevated accumulation of the membrane attack complex (MAC) in the choriocapillaris and degeneration of macular choriocapillaris endothelial cells (ECs). Thus, one could reasonably conclude that the endothelial cell death that occurs in AMD is due to injury by the MAC. We therefore sought to identify strategies for protecting ECs against MAC lysis. RF/6A endothelial cells were pre-incubated with a library of FDA-approved small molecules, followed by incubation with complement intact human serum quantification of cell death. Two closely related molecules identified in the screen, econazole nitrate and miconazole nitrate, were followed in validation and mechanistic studies. Both compounds reduced lysis of choroidal ECs treated with complement-intact serum, across a range of doses from 1 to 100 µM. Cell rescue was confirmed in mouse primary choroidal ECs. Both exosome release and cell surface roughness (assessed using a Holomonitor system) were reduced by drug pretreatment in RF/6A cells, whereas endosome formation increased with both drugs, consistent with imidazole-mediated alterations of cell surface dynamics. The results in the current study provide further proof of principle that small molecules can protect choroidal ECs from MAC-induced cell death and suggest that FDA approved compounds may be beneficial in reducing vascular loss and progression of AMD.

Details

Language :
English
ISSN :
2045-2322
Volume :
8
Issue :
1
Database :
MEDLINE
Journal :
Scientific reports
Publication Type :
Academic Journal
Accession number :
30190604
Full Text :
https://doi.org/10.1038/s41598-018-31846-z