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. 2021 Jan 20;27:61–77.

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Copyright © 2021 Molecular Vision.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited, used for non-commercial purposes, and is not altered or transformed.

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Immunocytochemistry for F-actin, α-SMA, COL1A1, and fibronectin in hTM cells treated with ATX and LPA. A: Immunostaining for α-SMA (green) and COL1A1 (red) merged with 4’,6-diamidino-2-phenylindole (DAPI; blue) at 3, 6, and 24 h after treatment with 40 μM autotaxin (ATX) or 10 μM lysophosphatidic acid (LPA). LPA induced upregulation of α-SMA or COL1A1 from 3 h after treatment, and ATX induced upregulation of α-SMA or COL1A1 from 6 h after treatment. The ATX inhibitor, the LPAR antagonist, and the ROCK inhibitor statistically significantly attenuated these changes. B: Immunostaining for fibronectin (green) and F-actin (red) merged with DAPI (blue) at 3, 6, and 24 h after treatment with ATX or LPA. LPA and ATX induced upregulation of fibronectin from 3 h after treatment, and the ATX inhibitor, the LPAR antagonist, and the ROCK inhibitor attenuated these changes. Bar, 200 µm.