Keller Kate E

Johns Kassidy L, Faralli Jennifer A, Filla Mark S, Shah Nandini S, Sun Ying Ying, Keller Kate E et al.

Older TM cells show altered integrins (decreased α5, increased activated αvβ3), leading to enhanced contraction and fibrotic changes. This suggests an early age-related mechanism for glaucoma development.

Yang Yong-Feng, Holden Paul, Sun Ying Ying, Faralli Jennifer A, Peters Donna M, Keller Kate E

Glaucoma-affected trabecular meshwork cells show increased fibrosis markers and EndMT, suggesting these processes contribute to outflow obstruction, offering potential therapeutic targets for glaucoma.

Su Chien-Chia, Desikan Vaibhav, Betsch Kevin, Shim Myoung Sup, Keller Kate E, Liton Paloma B

Studying TM cells, researchers found mechanical stress increases tubulin acetylation, stabilizing microtubules. This process, elevated in glaucoma, can lower IOP, suggesting tubulin acetylation as a glaucoma therapeutic target.

Lozano Diana C, Yang Yong-Feng, Cepurna William O, Smoody Barbara F, Ing Eliesa, Morrison John C et al.

This rat study found elevated IOP alters gene expression in the trabecular meshwork (TGFβ pathway downregulated) and optic nerve head (immune/defense pathways upregulated), suggesting distinct tissue responses to pressure that may impact glaucoma.

Keller Kate E, Peters Donna M

This review highlights that trabecular meshwork ECM dysfunction increases outflow resistance and intraocular pressure, a primary glaucoma risk factor, by altering tissue structure and cell behavior.

Acott Ted S, Vranka Janice A, Keller Kate E, Raghunathan VijayKrishna, Kelley Mary J

Glaucoma involves impaired IOP homeostasis due to TM cell loss and stiffer outflow pathways. Normal eyes actively regulate outflow resistance; restoring TM cells can restore this, offering therapeutic insights.

Sun Ying Ying, Bradley John M, Keller Kate E

Glaucomatous trabecular meshwork cells exhibit altered, less dynamic tunneling nanotubes with slower signal transfer, suggesting impaired cellular communication crucial for intraocular pressure regulation in glaucoma.

Sun Ying Ying, Yang Yong-Feng, Keller Kate E

Silencing Myosin-X, which forms tunneling nanotubes, significantly reduced outflow facility in eye models, suggesting these structures are crucial for normal intraocular pressure regulation and may influence ECM degradation.

Jayaram Hari, Lozano Diana C, Johnson Elaine C, Choe Tiffany E, Cepurna William O, Saugstad Julie A et al.

Keller Kate E, Bradley John M, Sun Ying Ying, Yang Yong-Feng, Acott Ted S

TM cells use tunneling nanotubes to directly communicate signals and materials, potentially enhancing long-distance signaling in aqueous humor outflow regulation, impacting glaucoma mechanisms.

Jayaram Hari, Phillips Jay I, Lozano Diana C, Choe Tiffany E, Cepurna William O, Johnson Elaine C et al.

This pilot study found specific miRNAs in aqueous humor differ in glaucoma patients versus controls, suggesting their potential as novel biomarkers for POAG.

Keller Kate E, Vranka Janice A, Haddadin Ramez I, Kang Min-Hyung, Oh Dong-Jin, Rhee Douglas J et al.

Studying Tenascin C (TNC) in the eye's drain, researchers found that reducing TNC did not impact fluid outflow resistance or intraocular pressure, suggesting it doesn't directly cause glaucoma.

Keller Kate E, Sun Ying Ying, Yang Yong-Feng, Bradley John M, Acott Ted S

This study found HA synthesized by HAS1 and HAS2 contributes to human outflow resistance, while HAS3 does not, highlighting HA's significant role in glaucoma pathogenesis.

Keller Kate E, Bradley John M, Vranka Janice A, Acott Ted S

Studying versican in the trabecular meshwork, researchers found its levels inversely correlate with outflow, and silencing it alters outflow facility, suggesting its critical role in glaucoma.

Keller Kate E, Bradley John M, Acott Ted S

This study found ADAMTS-4, unlike -1 and -5, significantly increased outflow facility in the trabecular meshwork. This suggests ADAMTS-4 is a key regulator and potential therapeutic target for glaucoma.

Aga Mini, Bradley John M, Keller Kate E, Kelley Mary J, Acott Ted S

TM cells possess specialized structures (PILS) that actively degrade extracellular matrix. This focal ECM turnover likely helps regulate aqueous outflow and intraocular pressure, impacting glaucoma.

Keller Kate E, Bradley John M, Kelley Mary J, Acott Ted S

Disrupting glycosaminoglycan (GAG) biosynthesis increased aqueous humor outflow facility in human and porcine eyes, confirming GAGs critically regulate outflow resistance, potentially offering new glaucoma treatment targets.

Keller Kate E, Kelley Mary J, Acott Ted S

Stretching trabecular meshwork cells alters ECM gene expression and induces alternative splicing, producing novel protein isoforms. This impacts ECM remodeling crucial for intraocular pressure regulation.