Immune complex-induced, nitric oxide-mediated vascular endothelial cell death by phagocytes is prevented with decoy Fcγreceptors

3Citations
Citations of this article
10Readers
Mendeley users who have this article in their library.

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 (FcγRs) 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 FcγRs and ICs prevents endothelium damage. Herein, we demonstrate that dimeric FcγRIgs prevented nitric oxide (NO) mediated apoptosis of human umbilical vein endothelial cells (HUVECs) in an in vitro vasculitis model. Dimeric FcγR-Igs significantly inhibited the IC-induced upregulation of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) release by murine monocytic cell line. However, FcγR-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 FcγRs.

Cite

CITATION STYLE

APA

Mula, R. V. R., Machiah, D., Holland, L., Wang, X., Parihar, H., Sharma, A. C., … Shashidharamurthy, R. (2016). Immune complex-induced, nitric oxide-mediated vascular endothelial cell death by phagocytes is prevented with decoy Fcγreceptors. PLoS ONE, 11(4). https://doi.org/10.1371/journal.pone.0153620

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free