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. 2019 Dec 10;20(24):6216. doi: 10.3390/ijms20246216

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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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Aldh2 deficiency in BMMCs enhances the phosphorylation and activity of Kit and concomitantly increases ROS and reduces Shp-1 activity. Changes in Kit phosphorylation in cell lysates (A) and activity in Kit immunoprecipitates (B) after stimulation with 100 ng/mL SCF for various times in Aldh2^+/+ and Aldh2^−/− BMMCs, as indicated. (C) Shp-1 activity in immunoprecipitates from Aldh2^+/+ and Aldh2^−/− BMMCs stimulated with 100 ng/mL SCF for the indicated times. (D) Intracellular ROS levels in Aldh2^+/+ and Aldh2^−/− BMMCs treated with 100 ng/mL SCF for the indicated times. Data in (A–D) are the mean ± SEM of three independent cultures. (E) Treatment with increasing concentrations of the antioxidant TEMPO reverses the reduced Shp-1 activation in SCF (100 ng/mL)-stimulated Aldh2^−/− BMMCs. Data are the mean ± SEM of three independent experiments. * p < 0.05; ** p < 0.01; n.s; not significant.