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Updated: Jan 17, 2026

Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye
Published on: June 20, 2015
Integrin β1 mediates mechanosensitive regulation of human trabecular meshwork cell functions in response to substrate
Dongyan Li1, Ruotian Du1, Jilong Li1
1Key Laboratory of Biomechanics and Mechanobiology, Ministry of Education, National Medical Innovation Platform for Industry-Education Integration in Advanced Medical Devices (Interdiscipline of Medicine and Engineering), School of Biological Science and Medical Engineering, Beihang University, Beijing 100191, China.
Abstract:
Increased extracellular matrix (ECM) stiffness is a well-recognized pathological hallmark of the trabecular meshwork (TM) in glaucomatous eyes; however, the mechanotransductive pathways by which TM cells sense and respond to mechanical cues remain incompletely understood. In this study, we identified integrin β1 as a key stiffness-responsive molecule, with its fluorescence signal and membrane localization significantly enhanced in human trabecular meshwork cells (hTMCs) cultured on stiffer substrates. Functional blockade of integrin β1 led to a marked reduction in cell proliferation, migration, and phagocytic activity across all stiffness conditions. Notably, the magnitude of blocking effects varied with substrate stiffness: inhibition of proliferative and migratory capacities was more pronounced on rigid substrates, whereas blockade-induced reduction in phagocytic activity was more evident on compliant substrates. These findings suggest that integrin β1 plays a central role in mediating hTMCs responses to biomechanical signals and may contribute to the functional impairment of the TM outflow pathway in the pathogenesis of glaucoma.
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