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Original Research ARTICLE Provisionally accepted The full-text will be published soon. Notify me

Front. Pharmacol. | doi: 10.3389/fphar.2019.01373

C16 peptide promotes vascular growth and reduces inflammation in a neuromyelitis optica model

  • 1School of Medicine, Jinhua Polytechnic, China
  • 2Department of Anatomy and Cell Biology, School of Medicine, Zhejiang University, China

The goal of this study was to elucidate the mechanism of action of C16, a laminin-1 peptide that competes with αvβ3 for integrin binding, in treating neuromyelitis optica (NMO). A neuromyelitis optica (NMO) rat model was established and specific inhibitors were used to investigate the effect of Tie2 kinase, integrin, and PI3K/Akt signaling pathways on C16 function in NMO using histological, immunohistochemical, immunofluorescence, western blot, and ELISA assays. A total of 135 rats were divided into 5 groups: control untreated group (n =15) and 4 test groups (n = 30 per group) including vehicle treated control, C16, Tie2 kinase inhibitor + C16, and PI3K/Akt inhibitor LY294002 + C16. We found that inhibiting Tie2 kinase resulted in partial loss of C16 peptide-mediated effects, while suppressing PI3K/Akt signaling reduced C16 peptide-mediated effects. In addition, activation of the αvβ3 integrin axis and Tie2 kinase promoted PI3K/Akt signaling. Our study showed that the Tie2-PI3K/Akt, Tie2-integrin, and integrin-PI3K/Akt signaling pathways regulate C16 peptide function in vascular growth and stabilization as well as inflammation in NMO.

Keywords: C16 peptide, receptor tyrosine kinase Tie2, PI3K/Akt pathways, αvβ3 integrin, Neuromyelitis optica (NMO)

Received: 27 Jul 2019; Accepted: 29 Oct 2019.

Copyright: © 2019 Chen, Fu, Jiang and Han. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Mx. Shu Han, Department of Anatomy and Cell Biology, School of Medicine, Zhejiang University, Hangzhou, China,