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CRISPR-Cas9-based treatment of myocilin-associated glaucoma
Journal article   Open access   Peer reviewed

CRISPR-Cas9-based treatment of myocilin-associated glaucoma

Ankur Jain, Gulab Zode, Ramesh B Kasetti, Fei A Ran, Winston Yan, Tasneem P Sharma, Kevin Bugge, Charles C Searby, John H Fingert, Feng Zhang, …
Proceedings of the National Academy of Sciences - PNAS, Vol.114(42), pp.11199-11204
10/17/2017
DOI: 10.1073/pnas.1706193114
PMCID: PMC5651749
PMID: 28973933
url
https://doi.org/10.1073/pnas.1706193114View
Published (Version of record) Open Access

Abstract

Primary open-angle glaucoma (POAG) is a leading cause of irreversible vision loss worldwide, with elevated intraocular pressure (IOP) a major risk factor. Myocilin ( ) dominant gain-of-function mutations have been reported in ∼4% of POAG cases. mutations result in protein misfolding, leading to endoplasmic reticulum (ER) stress in the trabecular meshwork (TM), the tissue that regulates IOP. We use CRISPR-Cas9-mediated genome editing in cultured human TM cells and in a MYOC mouse model of POAG to knock down expression of mutant MYOC, resulting in relief of ER stress. In vivo genome editing results in lower IOP and prevents further glaucomatous damage. Importantly, using an ex vivo human organ culture system, we demonstrate the feasibility of human genome editing in the eye for this important disease.
Glycoproteins - genetics Cell Line Cytoskeletal Proteins - genetics Glaucoma, Open-Angle - genetics Humans Gene Editing Glaucoma, Open-Angle - therapy Animals CRISPR-Cas Systems Mice Eye Proteins - genetics In Vitro Techniques Genetic Therapy - methods

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