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Article: An in vitro pressure model towards studying the response of primary retinal ganglion cells to elevated hydrostatic pressures

TitleAn in vitro pressure model towards studying the response of primary retinal ganglion cells to elevated hydrostatic pressures
Authors
Issue Date2019
PublisherNature Research (part of Springer Nature): Fully open access journals. The Journal's web site is located at http://www.nature.com/srep/index.html
Citation
Scientific Reports, 2019, v. 9 n. 1, p. article no. 9057 How to Cite?
AbstractGlaucoma is a leading cause of blindness characterized by progressive degeneration of retinal ganglion cells (RGCs). A well-established risk factor for the development and progression of glaucoma is elevation of intraocular pressure (IOP). However, how elevated IOP leads to RGC degeneration remains poorly understood. Here, we fabricate a facile, tunable hydrostatic pressure platform to study the effect of increased hydrostatic pressure on RGC axon and total neurite length, cell body area, dendritic branching, and cell survival. The hydrostatic pressure can be adjusted by varying the height of a liquid reservoir attached to a three-dimensional (3D)-printed adapter. The proposed platform enables long-term monitoring of primary RGCs in response to various pressure levels. Our results showed pressure-dependent changes in the axon length, and the total neurite length. The proportion of RGCs with neurite extensions significantly decreased by an average of 38 ± 2% (mean ± SEM) at pressures 30 mmHg and above (p < 0.05). The axon length and total neurite length decreased at a rate of 1.65 ± 0.18 μm and 4.07 ± 0.34 μm, respectively (p < 0.001), for each mmHg increase in pressure after 72 hours pressure treatment. Dendritic branching increased by 0.20 ± 0.05 intersections/day at pressures below 25 mmHg, and decreased by 0.07 ± 0.01 intersections/day at pressures above 25 mmHg (p < 0.001). There were no significant changes in cell body area under different levels of hydrostatic pressure (p ≥ 0.05). Application of this model will facilitate studies on the biophysical mechanisms that contribute to the pathophysiology of glaucoma and provide a channel for the screening of potential pharmacological agents for neuroprotection.
Persistent Identifierhttp://hdl.handle.net/10722/272901
ISSN
2017 Impact Factor: 4.122
2015 SCImago Journal Rankings: 2.073
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorWU, J-
dc.contributor.authorMak, HK-
dc.contributor.authorChan, YK-
dc.contributor.authorLin, C-
dc.contributor.authorKONG, C-
dc.contributor.authorLeung, CKS-
dc.contributor.authorShum, HC-
dc.date.accessioned2019-08-06T09:18:43Z-
dc.date.available2019-08-06T09:18:43Z-
dc.date.issued2019-
dc.identifier.citationScientific Reports, 2019, v. 9 n. 1, p. article no. 9057-
dc.identifier.issn2045-2322-
dc.identifier.urihttp://hdl.handle.net/10722/272901-
dc.description.abstractGlaucoma is a leading cause of blindness characterized by progressive degeneration of retinal ganglion cells (RGCs). A well-established risk factor for the development and progression of glaucoma is elevation of intraocular pressure (IOP). However, how elevated IOP leads to RGC degeneration remains poorly understood. Here, we fabricate a facile, tunable hydrostatic pressure platform to study the effect of increased hydrostatic pressure on RGC axon and total neurite length, cell body area, dendritic branching, and cell survival. The hydrostatic pressure can be adjusted by varying the height of a liquid reservoir attached to a three-dimensional (3D)-printed adapter. The proposed platform enables long-term monitoring of primary RGCs in response to various pressure levels. Our results showed pressure-dependent changes in the axon length, and the total neurite length. The proportion of RGCs with neurite extensions significantly decreased by an average of 38 ± 2% (mean ± SEM) at pressures 30 mmHg and above (p < 0.05). The axon length and total neurite length decreased at a rate of 1.65 ± 0.18 μm and 4.07 ± 0.34 μm, respectively (p < 0.001), for each mmHg increase in pressure after 72 hours pressure treatment. Dendritic branching increased by 0.20 ± 0.05 intersections/day at pressures below 25 mmHg, and decreased by 0.07 ± 0.01 intersections/day at pressures above 25 mmHg (p < 0.001). There were no significant changes in cell body area under different levels of hydrostatic pressure (p ≥ 0.05). Application of this model will facilitate studies on the biophysical mechanisms that contribute to the pathophysiology of glaucoma and provide a channel for the screening of potential pharmacological agents for neuroprotection.-
dc.languageeng-
dc.publisherNature Research (part of Springer Nature): Fully open access journals. The Journal's web site is located at http://www.nature.com/srep/index.html-
dc.relation.ispartofScientific Reports-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleAn in vitro pressure model towards studying the response of primary retinal ganglion cells to elevated hydrostatic pressures-
dc.typeArticle-
dc.identifier.emailChan, YK: josephyk@connect.hku.hk-
dc.identifier.emailShum, HC: ashum@hku.hk-
dc.identifier.authorityChan, YK=rp02536-
dc.identifier.authorityShum, HC=rp01439-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1038/s41598-019-45510-7-
dc.identifier.pmid31227762-
dc.identifier.pmcidPMC6588599-
dc.identifier.scopuseid_2-s2.0-85067799663-
dc.identifier.hkuros300876-
dc.identifier.volume9-
dc.identifier.issue1-
dc.identifier.spagearticle no. 9057-
dc.identifier.epagearticle no. 9057-
dc.publisher.placeUnited Kingdom-

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