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. 2019 Dec 20;9(1):28. doi: 10.3390/cells9010028

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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(A,B) OSM-dependent chemotaxis relies on ROS intracellular generation. Boyden’s chamber assay (A) was performed on LX2 cells treated with hrOSM 10 ng/mL for 6 h or, where indicated, pre-treated for 1 h with the pharmacological inhibitor of the NADPH oxidase (APO: apocynin 250 µM) or with the JAK2 inhibitor (AG490 100 µM) and then exposed or not to hrOSM 10 ng/mL for 6 h. * p < 0.05, versus control value, # p < 0.05 versus OSM value. (B) Representative images of cells on filter from Boyden’s chamber assay stained with crystal violet. Original magnification is indicated. (C,D) OSM-dependent non-oriented migration relies on STATI 1/3 activation. Wound healing assay (C) was performed on LX2 cells treated with hrOSM 10 ng/mL for 20 h or, where indicated, pre-treated for 1 h with the the pharmacological inhibitor of the NADPH oxidase (APO: apocynin 250 µM) or with the JAK2 inhibitor (AG490 100 µM) and then exposed or not to hrOSM 10 ng/mL for 20 h. * p < 0.05, versus control value, # p < 0.05 versus OSM value. (D) Representative images of cells invading the artificial wound stained with crystal violet. Original magnification is indicated.

(A,B) OSM-dependent chemotaxis relies on ROS intracellular generation. Boyden’s chamber assay (A) was performed on LX2 cells treated with hrOSM 10 ng/mL for 6 h or, where indicated, pre-treated for 1 h with the pharmacological inhibitor of the NADPH oxidase (APO: apocynin 250 µM) or with the JAK2 inhibitor (AG490 100 µM) and then exposed or not to hrOSM 10 ng/mL for 6 h. * p < 0.05, versus control value, # p < 0.05 versus OSM value. (B) Representative images of cells on filter from Boyden’s chamber assay stained with crystal violet. Original magnification is indicated. (C,D) OSM-dependent non-oriented migration relies on STATI 1/3 activation. Wound healing assay (C) was performed on LX2 cells treated with hrOSM 10 ng/mL for 20 h or, where indicated, pre-treated for 1 h with the the pharmacological inhibitor of the NADPH oxidase (APO: apocynin 250 µM) or with the JAK2 inhibitor (AG490 100 µM) and then exposed or not to hrOSM 10 ng/mL for 20 h. * p < 0.05, versus control value, # p < 0.05 versus OSM value. (D) Representative images of cells invading the artificial wound stained with crystal violet. Original magnification is indicated.