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. 2020 Sep 24;10:15641. doi: 10.1038/s41598-020-72779-w

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© The Author(s) 2020

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Schematic representation of the effect of GIMs on TGFβ signaling in hTM cells with or without exogenous TGFβ2. (Left cellular compartment) In the absence of exogenous TGFβ2 or DEX, GIMs activate non-Smad TGFβ2 signaling in correlation with increased expression/activity of specific ECM structural, matricellular, and crosslinking genes/proteins in hTM cells. Imbalances in genes/proteins responsible for ECM turnover (MMPs and TIMP2) lead to impaired ECM degradation, increased ECM deposition and stiffness associated with ocular hypertension. (Right cellular compartment) In the presence of exogenous TGFβ2, GIMs potentiate Smad and non-Smad TGFβ2 signaling in association with actin cytoskeletal and more pronounced ECM changes in hTM cells. Concurrent dysregulated ECM turnover (increased MMPs and TIMPs) results in more pronounced ECM accumulation and stiffness implicated in ocular hypertension. rhTGFβ2 recombinant human transforming growth factor beta 2. DEX Dexamethasone. GIM glucocorticoid-induced cell-derived matrix. ECM Extracellular matrix. eTGFβ2 ECM-derived TGFβ2. TGFβR TGFβ receptor complex. hTM Human trabecular meshwork. MMPs Matrix metalloproteinases. TIMPs Tissue inhibitor of matrix metalloproteinases. CTGF Connective tissue growth factor.