Effect of VEGF receptor inhibitors on TEER in SCE cell monolayers.

<p>SCE cells were treated with VEGF121 with or without axitinib (A), Ki8751 (B), or ZM306416 (C) for 48 h. Data are expressed as the mean ± SD from six (A, B) or eight (C) separate filters. *<i>P</i> < 0.05 and **<i>P</i> < 0.01 using the Tukey–Kramer HSD test.</p

The Effect of VEGF165 on TEER in SCE Cells.

<p>The Effect of VEGF165 on TEER in SCE Cells.</p

The Effect of VEGF121 on Outflow Facility in Porcine Eyes.

<p>The Effect of VEGF121 on Outflow Facility in Porcine Eyes.</p

Effect of VEGF121 or VEGF165 on cell shape, F-actin structure, and junctional proteins in SCE cells.

<p>VEGF121 or VEGF165 were used to treat SCE cells for 48 h. The top panels show the phase contrast images and the middle panels show the F-actin-stained images (red). Cell nuclei were counterstained with 4',6-diamidino-2-phenylindole (DAPI, blue, middle panel). Bottom panels show a related molecule (ZO-1, green) involved in cell-cell contact. Scale bar, 100 μm.</p

Effect of VEGF121 or VEGF165 on the cell shape and F-actin structure in TM cells.

<p>VEGF121 or VEGF165 were used to treat TM cells for 48 h. The top panels show the phase contrast images and the bottom panels show the F-actin-stained images (red). Scale bar, 100 μm.</p

The Effect of VEGF165 on TEER in TM Cells.

<p>The Effect of VEGF165 on TEER in TM Cells.</p

The Effect of VEGF121 on TEER in SCE Cells.

<p>The Effect of VEGF121 on TEER in SCE Cells.</p

Effect of VEGF121 or VEGF165 on TEER in TM cell monolayers.

<p>TM cells were treated with VEGF121 (A, B) or VEGF165 (C, D) for 48 h. (A, C) The time course of TEER changes after 30 ng/mL VEGF121 (A) or VEGF165 (C) treatment. (B, D) TEER changes after VEGF121 (B) or VEGF165 (D) treatment for 48 h. Data are expressed as the mean ± SD from six separate filters (n = 6).</p

Effect of perfusion with VEGF121 on outflow facility.

<p>The anterior segments of porcine eyes were perfused with 30 ng/mL VEGF121 at a constant flow of 3 μL/min at 37°C for 48 h. Data of outflow facility are expressed as the percent change from the baseline value, and expressed as the mean (n = 5).</p

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

<div><p>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 <i>COL1A2</i>. 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.</p></div