ArticlePloS one2024
Digital spatial profiling of segmental outflow regions in trabecular meshwork reveals a role for ADAM15.
Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 2 citations in OpenAlex.
- Transcriptomic Profiling of High vs. Low Flow Regions of Mouse and Human Trabecular Meshwork.bioRxiv : the preprint server for biology · 2026Article
- Transcriptomic Atlas of Human Trabecular Meshwork Uncovers the Cellular Landscape and Provides Insights into Glaucoma Pathophysiology.Research square · 2026Article
- Segmental Outflow and Trabecular Meshwork Stiffness in an Ocular Hypertensive Mouse Model.Investigative ophthalmology & visual science · 2026Article
- Cholinergic Improvement of Low-Flow Segmental Aqueous Humor Outflow in Humans.Ophthalmology science · 2026Article
- Segmental outflow and trabecular meshwork stiffness in an ocular hypertensive mouse model.bioRxiv : the preprint server for biology · 2026Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
In this study we used a spatial transcriptomics approach to identify genes specifically associated with either high or low outflow regions in the trabecular meshwork (TM) that could potentially affect aqueous humor outflow in vivo. High and low outflow regions were identified and isolated from organ cultured human anterior segments perfused with fluorescently-labeled 200 nm FluoSpheres. The NanoString GeoMx Digital Spatial Profiler (DSP) platform was then used to identified genes in the paraffin embedded tissue sections from within those regions. These transcriptome analyses revealed that 16 genes were statistically upregulated in high outflow regions and 57 genes were statistically downregulated in high outflow regions when compared to low outflow regions. Gene ontology enrichment analysis indicated that the top three biological categories of these differentially expressed genes were ECM/cell adhesion, signal transduction, and transcription. The ECM/cell adhesion genes that showed the largest differential expression (Log2FC ±1.5) were ADAM15, BGN, LDB3, and CRKL. ADAM15, which is a metalloproteinase that can bind integrins, was upregulated in high outflow regions, while the proteoglycan BGN and two genes associated with integrin signaling (LDB3, and CRKL) were downregulated. Immunolabeling studies supported the differential expression of ADAM15 and showed that it was specifically upregulated in high outflow regions along the inner wall of Schlemm's canal and in the juxtacanalicular (JCT) region of the TM. In addition to these genes, the studies showed that genes for decorin, a small leucine-rich proteoglycan, and the α8 integrin subunit were enriched in high outflow regions. These studies identify several novel genes that could be involved in segmental outflow, thus demonstrating that digital spatial profiling could be a useful approach for understanding segmental flow through the TM. Furthermore, this study suggests that changes in the expression of genes involved in regulating the activity and/or organization of the ECM and integrins in the TM are likely to be key players in segmental outflow.
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