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. 2020 Mar 19;13:38. doi: 10.1186/s13041-020-00573-w

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 5 — Relationships between NOTCH3, PDGFRβ and migration. a Cell covered area was measured at 9 h after the start of migration assay. Both NOTCH3 and PDGFRB knockdown resulted in the reduced migration rate in CADASIL iPSMCs (CAD1–1 N3 and Pβ) to the control level (TIG114 Cont). However, NOTCH3 knockdown resulted in further increase of PDGFRβ in CADASIL, while inhibition of DAPT treatment significantly reduced expression (b). c Immunofluorescent staining of PDGFRβ revealed increased surface and cytoplasmic PDGFRβ in CADASIL MCs (CAD1–1 control, Live and Fixed). Further increase of PDGFRβ by NOTCH3 siRNA transfection (N3KD) was explained by the intracellular aggregation of excessive PDGFRβ (arrowheads) and reduced functional receptors on the plasma membrane (CAD1–1 N3KD, fixed). Bar represents 20 μm. The error bars represent the SEM. *p < 0.05, **p < 0.01