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Abstract #60687 Published in IGR 16-4

p38 MAP Kinase Inhibitor Suppresses Transforming Growth Factor-β2-Induced Type 1 Collagen Production in Trabecular Meshwork Cells

Inoue-Mochita M; Inoue T; Fujimoto T; Kameda T; Awai-Kasaoka N; Ohtsu N; Kimoto K; Tanihara H
PLoS ONE 2015; 10: e0120774

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Glaucoma is an age-related neurodegenerative disease of retinal ganglion cells, and appropriate turnover of the extracellular matrix in the trabecular meshwork is important in its pathology. Here, we report the effects of Rho-associated kinase (ROCK) and p38 MAP kinase on transforming growth factor (TGF)-β2-induced type I collagen production in human trabecular meshwork cells. TGF-β2 increased RhoA activity, actin polymerization, and myosin light chain 2 phosphorylation. These effects were significantly inhibited by Y-27632, but not SB203580. TGF-β2 also increased promoter activity, mRNA synthesis, and protein expression of COL1A2. These effects were significantly inhibited by SB203580, but not Y-27632. Additionally, Y-27632 did not significantly inhibit TGF-β2-induced promoter activation, or phosphorylation or nuclear translocation of Smad2/3, whereas SB203580 partially suppressed these processes. Collectively, TGF-β2-induced production of type 1 collagen is suppressed by p38 inhibition and accompanied by partial inactivation of Smad2/3, in human trabecular meshwork cells.

Department of Ophthalmology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.

Full article

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Classification:

2.5.1 Trabecular meshwork (Part of: 2 Anatomical structures in glaucoma > 2.5 Meshwork)
3.6 Cellular biology (Part of: 3 Laboratory methods)
3.5 Molecular biology incl. SiRNA (Part of: 3 Laboratory methods)

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