# Incision of the pre-Descemet layer and Descemet membrane affects outflow facility: ex-vivo studies on a human eye perfusion model

**Authors:** Prity Sahay, Burçin Kepez Yildiz, Perla Filippini, Imran Masood, Harminder Singh Dua

PMC · DOI: 10.3389/fmed.2026.1706969 · Frontiers in Medicine · 2026-02-06

## TL;DR

This study shows that incising the pre-Descemet layer and Descemet membrane in human eyes reduces aqueous outflow, increasing eye pressure due to changes in the trabecular meshwork.

## Contribution

The study demonstrates a novel link between surgical disruption of the PDL/DM and increased outflow resistance via biomechanical and molecular changes in the TM.

## Key findings

- Incising the PDL and DM decreased outflow rate and increased resistance in the ASPM model.
- Incised eyes showed increased fibronectin, myocilin, and alpha-smooth muscle actin in the TM.
- Active MMP-9 levels in perfusates increased on day 4 but decreased by day 9 in experimental eyes.

## Abstract

The collagen and elastin fibres of the pre-Descemet layer or Dua layer (PDL) fan out to become the beams of the trabecular meshwork (TM), indicating similarities in the structural elements in the PDL and TM. This study evaluated the effects of disruption of the PDL and Descemet membrane (DM) on the facility of aqueous outflow from the anterior chamber, using human eyes and an anterior segment perfusion model (ASPM).

The ASPM was established using human donor eyes. The PDL and DM in the experimental eyes were half incised circumferentially along an 8 mm diameter circle for 180°, and the other half was left non-incised.

The experimental eyes in the ASPM model exhibited a decrease in the outflow rate, indicating an increased outflow resistance. In the TM, the expressions of fibronectin, myocilin and alpha-smooth muscle actin were increased in incised compared to non-incised and control samples. The outflow perfusates in the experimental eyes showed a significant increase in the level of active MMP-9 on day 4 and a subsequent decrease on day 9 compared to the control eyes. Myocilin was only detected in the perfusate on day 9 in the experimental eyes.

Our study suggests that surgical disruption of the PDL and DM results in decreased outflow, which can be due to an alteration in biomechanical properties, with consequent molecular changes in the TM, adversely affecting the resistance to outflow. This could explain why the incidence of raised pressure is greater with penetrating keratoplasty compared to deep anterior lamellar keratoplasty.

## Linked entities

- **Proteins:** fn1.S (fibronectin 1 S homeolog), myoc (myocilin, trabecular meshwork inducible glucocorticoid response), MMP9 (matrix metallopeptidase 9)
- **Species:** Homo sapiens (taxon 9606)

## Full-text entities

- **Genes:** MYOC (myocilin) [NCBI Gene 4653] {aka GLC1A, GPOA, JOAG, JOAG1, TIGR}, FN1 (fibronectin 1) [NCBI Gene 2335] {aka CIG, ED-B, FINC, FN, FNZ, GFND}, TIMP1 (TIMP metallopeptidase inhibitor 1) [NCBI Gene 7076] {aka CLGI, EPA, EPO, HCI, TIMP, TIMP-1}, MMP9 (matrix metallopeptidase 9) [NCBI Gene 4318] {aka CLG4B, GELB, MANDP2, MMP-9}, CDH2 (cadherin 2) [NCBI Gene 1000] {aka ACOGS, ADHD8, ARVD14, CD325, CDHN, CDw325}, SNAI2 (snail family transcriptional repressor 2) [NCBI Gene 6591] {aka SLUG, SLUGH, SLUGH1, SNAIL2, WS2D}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, ELN (elastin) [NCBI Gene 2006] {aka ADCL1, SVAS, WBS, WS}, ACTA1 (actin alpha 1, skeletal muscle) [NCBI Gene 58] {aka ACTA, ASMA, CFTD, CFTD1, CFTDM, CMYO2A}, MMP2 (matrix metallopeptidase 2) [NCBI Gene 4313] {aka CLG4, CLG4A, MMP-2, MMP-II, MONA, TBE-1}, VIM (vimentin) [NCBI Gene 7431]
- **Diseases:** DM (MESH:D015433), ocular hypertension (MESH:D009798), Glaucoma (MESH:D005901), Fibrotic protein (MESH:D011488), ASPM (MESH:C537775), TM (MESH:D000236), DALK (MESH:C535342), inflammation (MESH:D007249), PKP (MESH:D015807), optic nerve damage (MESH:D020221), raised eye pressure (MESH:D000085583), edema (MESH:D004487)
- **Chemicals:** steroid (MESH:D013256), BCA (MESH:C047117), sucrose (MESH:D013395), PFA (MESH:C003043), eosin (MESH:D004801), polyvinylidene fluoride (MESH:C024865), Coomassie blue (MESH:C048139), DAPI (MESH:C007293), OCT (-), H&amp;E (MESH:D006371), dextran (MESH:D003911), hematoxylin (MESH:D006416), ZnCl2 (MESH:C016837), Alexa Fluor 488 (MESH:C000711379), CaCl2 (MESH:D002122), SDS (MESH:D012967), acetic acid (MESH:D019342), NaCl (MESH:D012965), methanol (MESH:D000432), Triton X-100 (MESH:D017830), polyacrylamide (MESH:C016679)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Mutations:** C for 20-30, G170023307726X, G170023306708G

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12920517/full.md

## References

36 references — full list in the complete paper: https://tomesphere.com/paper/PMC12920517/full.md

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Source: https://tomesphere.com/paper/PMC12920517