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. 2021 May 3;121(9):1206–1219. doi: 10.1055/a-1497-9649

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The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. ( https://creativecommons.org/licenses/by-nc-nd/4.0/ )

This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License, which permits unrestricted reproduction and distribution, for non-commercial purposes only; and use and reproduction, but not distribution, of adapted material for non-commercial purposes only, provided the original work is properly cited.

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Fig. 7 — CDC42 mediated the effect of miR-204-5p on PLS. ( A ) CDC42 knock-down increased the adhesion of megakaryocytes in a fibrinogen-coated channel in dynamic conditions and ( B ) led to an actin cytoskeleton organization similar to that observed after miR-204-5p transfection with an increase in the stress-fiber content. Images were taken using confocal microscopy of megakaryocytes, with polylobed nucleus labeled with DAPI ( blue ) and F-actin labeled with TRITC-phalloidin ( red ) (scale bars = 20 μm). ( C ) Knock-down of CDC42 decreased the relative proPLS network area and ( D ) displayed a similar pattern to that observed after miR-204-5p transfection (Si-3000 camera, scale bars = 100 μm). ( E ) CDC42 silencing did not impact CD62P expression and ( F ) increased relative GPIIbIIIa expression in activated PLS and ( G and H ) enhanced the PLS spreading area on fibrinogen-coated coverslips (LSM700 microscope, scale bars = 20 μm). Results are expressed relative to the mock condition. n = 3 to 5 independent experiments; * p < 0.05, ** p < 0.01. PLS, platelet-like structure.