Document Type
Article
Publication Date
2016
Abstract
Autoimmune vasculitis is an endothelial inflammatory disease that results from the deposition of immune-complexes (ICs) in blood vessels. The interaction between Fcgamma receptors (FcyRs) expressed on inflammatory cells with ICs is known to cause blood vessel damage. Hence, blocking the interaction of ICs and inflammatory cells is essential to prevent the IC-mediated blood vessel damage. Thus we tested if uncoupling the interaction of FcyRs and ICs prevents endothelium damage. Herein, we demonstrate that dimeric FcyR-Igs prevented nitric oxide (NO) mediated apoptosis of human umbilical vein endothelial cells (HUVECs) in an in vitro vasculitis model. Dimeric FcyR-Igs significantly inhibited the IC-induced upregulation of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) release by murine monocytic cell line. However, FcyR-Igs did not affect the exogenously added NO-induced upregulation of pro-apoptotic genes such as Bax (15 fold), Bak (35 fold), cytochrome-C (11 fold) and caspase-3 (30 fold) in HUVECs. In conclusion, these data suggest that IC-induced NO could be one of the major inflammatory mediator promoting blood vessel inflammation and endothelial cell death during IC-mediated vasculitis which can be effectively blocked by dimeric decoy FcyRs.
Publication Title
PLoS ONE
Volume
11
Issue
4
First Page
e0153620
Recommended Citation
Mula, Ramanjaneya V. R.; Machiah, Deepa; Holland, Lauren; Wang, Xinyu; Parihar, Harish; Sharma, Avadhesh; Selvaraj, Periasamy; and Shashidharamurthy, Rangaiah, "Immune Complex-Induced, Nitric Oxide-Mediated Vascular Endothelial Cell Death by Phagocytes Is Prevented with Decoy FcyReceptors" (2016). PCOM Scholarly Papers. 1680.
https://digitalcommons.pcom.edu/scholarly_papers/1680
Comments
This article was published in PLoS ONE, Volume 11, Issue 4, Pages e0153620- .
The published version is available at http://dx.doi.org/10.1371/journal.pone.0153620.
Copyright © 2016 Mula et al.