Related Experiment Video
Updated: Jan 1, 2026
In Vitro Myelination of Peripheral Axons in a Coculture of Rat Dorsal Root Ganglion Explants and Schwann Cells
Published on: February 10, 2023
C16 Peptide Promotes Vascular Growth and Reduces Inflammation in a Neuromyelitis Optica Model
Haohao Chen1, Xiaoxiao Fu2, Jinzhan Jiang1
1Medical Molecular Biology Laboratory, School of Medicine, Jinhua Polytechnic, Jinhua, China.
Abstract:
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 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 150 rats were divided into five groups: a control untreated group (n = 18) and four test groups (n = 33 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.
Insights
C16 peptide treatment for neuromyelitis optica (NMO) involves Tie2 kinase and PI3K/Akt pathways. These pathways are crucial for C16
Area of Science:
- Neuroscience
- Immunology
- Molecular Biology
Background:
- Neuromyelitis optica (NMO) is a severe autoimmune disorder affecting the central nervous system.
- Laminin-1 derived peptide C16 shows therapeutic potential by targeting αvβ3 integrin binding.
Purpose of the Study:
- To elucidate the mechanism of action of C16 in treating NMO.
- To investigate the roles of Tie2 kinase, integrin, and PI3K/Akt signaling pathways in C16 function.
Main Methods:
- Established a NMO rat model for experimental studies.
- Utilized histological, immunohistochemical, immunofluorescence, Western blot, and ELISA assays.
- Administered specific inhibitors (Tie2 kinase inhibitor, PI3K/Akt inhibitor LY294002) alongside C16 treatment.
Main Results:
- Inhibition of Tie2 kinase partially reduced C16 peptide-mediated effects.
- Suppression of PI3K/Akt signaling significantly diminished C16 peptide-mediated effects.
- Activation of the αvβ3 integrin axis and Tie2 kinase promoted PI3K/Akt signaling.
Conclusions:
- The Tie2-PI3K/Akt, Tie2-integrin, and integrin-PI3K/Akt signaling pathways are critical regulators of C16 peptide function in NMO.
- C16 influences vascular stabilization and inflammation in NMO through these interconnected signaling pathways.
More Related Videos
10:50Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo
Published on: March 26, 2019
07:30A Simple Approach to Induce Experimental Autoimmune Neuritis in C57BL/6 Mice for Functional and Neuropathological Assessments
Published on: November 9, 2017