Further Support for ECM Control of Receptor Trafficking and Signaling

Lindsay Clegg; Feilim Mac Gabhann

doi:10.1002/jcp.25464

Further Support for ECM Control of Receptor Trafficking and Signaling

J Cell Physiol. 2017 Jan;232(1):36-7. doi: 10.1002/jcp.25464.

Authors

Lindsay Clegg^{1

2

3}, Feilim Mac Gabhann^{4

5

6

7}

Affiliations

¹ Institute for Computational Medicine, Johns Hopkins University, Baltimore, Maryland.
² Institute for NanoBioTechnology, Johns Hopkins University, Baltimore, Maryland.
³ Department of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland.
⁴ Institute for Computational Medicine, Johns Hopkins University, Baltimore, Maryland. feilim@jhu.edu.
⁵ Institute for NanoBioTechnology, Johns Hopkins University, Baltimore, Maryland. feilim@jhu.edu.
⁶ Department of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland. feilim@jhu.edu.
⁷ Department of Materials Science and Engineering, Johns Hopkins University, Baltimore, Maryland. feilim@jhu.edu.

PMID: 27323268
DOI: 10.1002/jcp.25464

Abstract

Recently, Sack et al. (2016) presented an interesting, novel data set in Journal of Cellular Physiology examining the effect of substrate stiffness on VEGF processing and signaling. The data represent a clear contribution to the field. However, the authors' conclusion that "extracellular matrix binding is essential for VEGF internalization" conflicts with other knowledge in the field, and is not supported by their data. Instead, their data demonstrate the effect of heparin addition and changing ECM stiffness on both VEGF binding to fibronectin and VEGF binding to endothelial receptors. This is consistent with other work showing that matrix binding reduces VEGF-VEGFR internalization, shifting downstream signaling. J. Cell. Physiol. 232: 36-37, 2017. © 2016 Wiley Periodicals, Inc.

Publication types

Editorial