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. 2019 Sep 11;9:13090. doi: 10.1038/s41598-019-49482-6

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Hypothetical representation of PrP^C-mediated Endo-MT-like change in the TM. Physiological role of PrP^C in the TM: (1) PrP^C is expressed on the plasma membrane of TM cells. (2) PrP^C maintains cell-ECM interactions by stabilizing β1-integrin and other proteins^5,7. Pathological implications: (1) Downregulation of PrP^C induces (2) aggregation of β1-integrin and (3) upregulation of fibronectin, collagen 1A, α-SMA, vimentin, and laminin, resulting in (4) increase in IOP and possibly POAG. AH: aqueous humor; PM: plasma membrane; Nu: nucleus.