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Wu et al. Vessel Plus 2017;1:137-44 Vessel Plus
DOI: 10.20517/2574-1209.2017.15
www.vpjournal.net
Original Article Open Access

Perivascular mast cells promote neointimal

elastin deposition and suppress chronic vein

graft restenosis in hyperlipidaemic mice

Junxi Wu , Catherine Lawrence , Roger M. Wadsworth , Simon Kennedy 2
1
1,3
1
1 Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, Glasgow G4 0RE, UK.
2 Institute of Cardiovascular and Medical Sciences, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8TA, UK.
3 The Queen’s Medical Research Institute, The University of Edinburgh, Edinburgh EH16 4TJ, UK.
Correspondence to: Dr. Junxi Wu, The Queen’s Medical Research Institute, The University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ,
UK. E-mail: junxi.wu@ed.ac.uk
How to cite this article: Wu J, Lawrence C, Wadsworth RM, Kennedy S. Perivascular mast cells promote neointimal elastin deposition and suppress
chronic vein graft restenosis in hyperlipidaemic mice. Vessel Plus 2017;1:137-44.

Dr. Junxi Wu is a research fellow at the BHF Centre for Cardiovascular Science in The University of Edinburgh. He
received his PhD in physiology and pharmacology in 2008 from the University of Strathclyde. His research focus
is macro- and micro-vascular injury and remodelling. He is also interested in vascular tissue engineering including
fabrication of bio-artificial blood vessels and fast vascularization for cell therapy and organ regeneration using
cross-disciplinary approaches.

ABSTRACT
Article history: Aim: Mast cells are versatile innate immune cells and are reported to promote vascular
Received: 11 May 2017 inflammation and neointimal lesion formation, thereby contributing to the development of
Accepted: 23 Jun 2017 vascular stenosis and atherosclerosis. However, it is not clear whether mast cells also regulate
Published: 26 Sep 2017 vascular matrix remodelling in established neointima. This study addressed the hypothesis that
perivascular mast cells regulate neointimal matrix remodelling using a mouse vein graft model.
Key words: Methods: The impact of mast cells on neointimal remodelling was investigated using mast
Mast cells, cell-deficient animals in both normolipidaemic (Kit W-sh/W-sh ) and hyperlipidaemic (apoE Kit W-sh/W-sh )
-/-
elastin, conditions. The effect of perivascular mast cells on vascular matrix remodelling, including
chronic restenosis, collagen and elastin deposition, was investigated using a local mast cell reconstitution method
neointima, that selectively repopulated mast cells around the carotid artery (where the vein graft was
vein graft inserted) in Kit W-sh/W-sh mice. Results: In normolipidaemic vein grafts (Kit W-sh/W-sh vs. the wild
type control C57BL/6J), collagen synthesis was not affected by mast cell deficiency at 4 weeks.
In contrast, neointimal elastin was reduced by 6.5-fold in mast cell-deficient Kit W-sh/W-sh mice,
which was prevented by perivascular mast cell reconstitution. Mast cell deficiency induced a
similar reduction in neointimal elastin in hyperlipidaemic mice (apoE Kit W-sh/W-sh vs. apoE ),
-/-
-/-
with a significant increase in cell proliferation and neointimal area at 4 weeks. Conclusion:
Mast cells appear to promote elastin deposition in vein grafts and this may lead to further
suppression of cell proliferation and neointimal thickening under hyperlipidaemic conditions.
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