Publication: Membrane trafficking and exocytosis are upregulated in port wine stain blood vessels
Authors
Yin, Rong ; Rice, Shawn J. ; Wang, Jinwei ; Gao, Lin ; Tsai, Joseph ; Anvari, Radean T. ; Zhou, Fang ; Liu, Xin ; Wang, Gang ; Tang, Yuxin ; Mihm Jr, Martin C. ; Belani, Chandra P. ; Chen, Dong Bao ; Nelson, J. Stuart ; Tan, Wenbin
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Publisher
Universidad de Murcia. Departamento de Biología Celular e Histología
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DOI
DOI: 10.14670/HH-18-051
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info:eu-repo/semantics/article
Description
Abstract
Introduction. Port wine stain (PWS) is
characterized as a progressive dilatation of immature
venule-like vasculatures which result from
differentiation-impaired endothelial cells. In this study,
we aimed to identify the major biological pathways
accounting for the pathogenesis of PWS.
Methods. Sequential windowed acquisition of all
theoretical fragment ion mass spectra (SWATH-MS) was
used to identify differentially expressed proteins in PWS
lesions, followed by confirmative studies with
immunohistochemistry, immunoblot and transmission
electron microscopy (TEM).
Results. 107 out of 299 identified proteins showed
differential expressions in PWS lesions as compared to
normal skin, mainly involving the functions of
biosynthesis, membrane trafficking, cytoskeleton and
cell adhesion/migration. The confirmative studies
showed that expressions of membrane trafficking/
exocytosis related proteins such as VAT1, IQGAP1,
HSC70, clathrin, perlecan, spectrin α1 and GDIR1 were
significantly increased in PWS blood vessels as
compared to normal ones. Furthermore, TEM studies
showed there is a significant upregulation of
extracellular vesicle exocytosis from PWS blood vessels
as compared to control.
Conclusions. The biological process of membrane
trafficking and exocytosis is enhanced in PWS blood
vessels. Our results imply that the extracellular vesicles
released by lesional endothelial cells may act as potential
intercellular signaling mediators to contribute to the
pathogenesis of PWS.
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Citation
Histology and Histopathology, Vol.34, nº5, (2019)
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