. Author manuscript; available in PMC: 2017 Apr 1.

Published in final edited form as: Arterioscler Thromb Vasc Biol. 2016 Aug 11;36(10):2048–2057. doi: 10.1161/ATVBAHA.116.307610

Table 2.

Cleavage of EC junctional molecules during inflammation

Molecule	Model	Mechanism	Functional implications	Refs
PECAM-1	Serum starvation (HUVECs, EOMA, BAECs)	Cleavage by caspases & shedding by MMPs	- None described	54

VE-Cadherin	fMLP stimulated neutrophils (HUVECs)	Cleavage by neutrophil elastase & Cathepsin G	- ↑ permeability - Support neutrophil TEM	56
	Thrombin stimulation (HUVECs)	Cleavage by ADAM-10	- ↑ permeability - Support T-cell migration	55
	TNF stimulation (HUVECs)	Cleavage dependent on tyrosine kinases, Src kinase & MMPs	- None described	30

JAM-A	PMA, TNFα+ IFNγ, PAF (HUVECs)	Cleavage by ADAM-10, ADAM-17	- ↓ EC migration - ↓ neutrophil TEM	57

JAM-B	HBMEC incubation with tumour-cell secreted supernatant	Cleavage by Cathepsin S	- ↑ TEM of brain metastatic tumour cells	58

JAM-C	LPS, IL1-β, IL-18, MIF, IL-17, TNF, PMA (HUVECs)	Cleavage by ADAM-10, ADAM-17	- Supports angiogenesis	65
JAM-C	Murine cremaster muscle I-R and local LTB4	Cleavage by NE as supported by presentation of NE to JAM-C via neutrophil Mac-1	- ↑ neutrophil rTEM	50