Extracellular matrix gene expression in human trabecular meshwork cells following mechanical fluid flow stimulation

• Published in: International journal of ophthalmology Vol. 15; no. 3; pp. 388 - 393
• Main Authors: Yoshida, Koichi, Kawai, Motofumi, Utsunomiya, Tsugiaki, Ishibazawa, Akihiro, Song, Young-Seok, Udo, Mariana Sayuri B, Tasaki, Yoshikazu, Yoshida, Akitoshi
• Format: Journal Article
• Language: English
• Published: China International Journal of Ophthalmology Press 18.03.2022; Press of International Journal of Ophthalmology (IJO PRESS)
• Subjects: aqueous humor; Basic Research; extracellular matrix; glaucoma; intraocular pressure; shear stress; trabecular meshwork; shear stress; intraocular pressure; aqueous humor; glaucoma; extracellular matrix; trabecular meshwork
• ISSN: 2222-3959; 2227-4898
• DOI: 10.18240/ijo.2022.03.03

To investigate changes in extracellular matrix (ECM) gene expression in human trabecular meshwork (HTM) cells in response to mechanical fluid flow stimulation. HTM cells were grown on a glass plate coated with 0.02% type I collagen (COL) and exposed to shear stress (0, 0.2, 1.0 dyne/cm ) for 12h. Changes in genes related to the ECM were evaluated by real-time reverse transcriptase-polymerase chain reaction. Phosphorylation of Smad2 protein was investigated by Western blotting. After mechanical stimulation, COL type 4 alpha 2, COL type 6 alpha 1, and fibronectin-1 mRNA were significantly higher than the static control ( <0.05, <0.05, and <0.01, respectively). The metalloproteinase-2 and plasminogen activator inhibitor-1 mRNA were significantly higher than the static control ( <0.05 and <0.01, respectively), while the differences in the tissue inhibitors of metalloproteinases-2 mRNA were not significant. The phosphorylation of Smad2 levels was significantly higher compared to the static control cells. Changes in the expressions of genes associated ECM metabolism result in HTM cells after mechanical stimulation. The mechanical stimulation of the aqueous humor to the trabecular meshwork may promote ECM turnover and contribute to intraocular pressure homeostasis.