Axonopathy precedes cell death in ocular damage mediated by blast exposure

Abstract Traumatic brain injuries (TBI) of varied types are common across all populations and can cause visual problems. For military personnel in combat settings, injuries from blast exposures (bTBI) are prevalent and arise from a myriad of different situations. To model these diverse conditions, w...

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Autores principales:	Nickolas A. Boehme, Adam Hedberg-Buenz, Nicole Tatro, Michael Bielecki, William C. Castonguay, Todd E. Scheetz, Michael G. Anderson, Laura M. Dutca
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/ccfdf23006a846fa89fdb7f62743a8b4
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spelling	oai:doaj.org-article:ccfdf23006a846fa89fdb7f62743a8b42021-12-02T15:56:50ZAxonopathy precedes cell death in ocular damage mediated by blast exposure10.1038/s41598-021-90412-22045-2322https://doaj.org/article/ccfdf23006a846fa89fdb7f62743a8b42021-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-90412-2https://doaj.org/toc/2045-2322Abstract Traumatic brain injuries (TBI) of varied types are common across all populations and can cause visual problems. For military personnel in combat settings, injuries from blast exposures (bTBI) are prevalent and arise from a myriad of different situations. To model these diverse conditions, we are one of several groups modeling bTBI using mice in varying ways. Here, we report a refined analysis of retinal ganglion cell (RGC) damage in male C57BL/6J mice exposed to a blast-wave in an enclosed chamber. Ganglion cell layer thickness, RGC density (BRN3A and RBPMS immunoreactivity), cellular density of ganglion cell layer (hematoxylin and eosin staining), and axon numbers (paraphenylenediamine staining) were quantified at timepoints ranging from 1 to 17-weeks. RNA sequencing was performed at 1-week and 5-weeks post-injury. Earliest indices of damage, evident by 1-week post-injury, are a loss of RGC marker expression, damage to RGC axons, and increase in glial markers expression. Blast exposure caused a loss of RGC somas and axons—with greatest loss occurring by 5-weeks post-injury. While indices of glial involvement are prominent early, they quickly subside as RGCs are lost. The finding that axonopathy precedes soma loss resembles pathology observed in mouse models of glaucoma, suggesting similar mechanisms.Nickolas A. BoehmeAdam Hedberg-BuenzNicole TatroMichael BieleckiWilliam C. CastonguayTodd E. ScheetzMichael G. AndersonLaura M. DutcaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-19 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Nickolas A. Boehme Adam Hedberg-Buenz Nicole Tatro Michael Bielecki William C. Castonguay Todd E. Scheetz Michael G. Anderson Laura M. Dutca Axonopathy precedes cell death in ocular damage mediated by blast exposure
description	Abstract Traumatic brain injuries (TBI) of varied types are common across all populations and can cause visual problems. For military personnel in combat settings, injuries from blast exposures (bTBI) are prevalent and arise from a myriad of different situations. To model these diverse conditions, we are one of several groups modeling bTBI using mice in varying ways. Here, we report a refined analysis of retinal ganglion cell (RGC) damage in male C57BL/6J mice exposed to a blast-wave in an enclosed chamber. Ganglion cell layer thickness, RGC density (BRN3A and RBPMS immunoreactivity), cellular density of ganglion cell layer (hematoxylin and eosin staining), and axon numbers (paraphenylenediamine staining) were quantified at timepoints ranging from 1 to 17-weeks. RNA sequencing was performed at 1-week and 5-weeks post-injury. Earliest indices of damage, evident by 1-week post-injury, are a loss of RGC marker expression, damage to RGC axons, and increase in glial markers expression. Blast exposure caused a loss of RGC somas and axons—with greatest loss occurring by 5-weeks post-injury. While indices of glial involvement are prominent early, they quickly subside as RGCs are lost. The finding that axonopathy precedes soma loss resembles pathology observed in mouse models of glaucoma, suggesting similar mechanisms.
format	article
author	Nickolas A. Boehme Adam Hedberg-Buenz Nicole Tatro Michael Bielecki William C. Castonguay Todd E. Scheetz Michael G. Anderson Laura M. Dutca
author_facet	Nickolas A. Boehme Adam Hedberg-Buenz Nicole Tatro Michael Bielecki William C. Castonguay Todd E. Scheetz Michael G. Anderson Laura M. Dutca
author_sort	Nickolas A. Boehme
title	Axonopathy precedes cell death in ocular damage mediated by blast exposure
title_short	Axonopathy precedes cell death in ocular damage mediated by blast exposure
title_full	Axonopathy precedes cell death in ocular damage mediated by blast exposure
title_fullStr	Axonopathy precedes cell death in ocular damage mediated by blast exposure
title_full_unstemmed	Axonopathy precedes cell death in ocular damage mediated by blast exposure
title_sort	axonopathy precedes cell death in ocular damage mediated by blast exposure
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/ccfdf23006a846fa89fdb7f62743a8b4
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Axonopathy precedes cell death in ocular damage mediated by blast exposure

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