Exploring the Mechanism of Action of the 6-[4-(1-cyclohexyl-1H-tetrazol-5-yl) butoxy]-3,4-dihydro-2-(1H)-quinolinone for Neurovascular Unit using iTRAQ Technology.

1 Exploring the Mechanism of Action of the 6-[4-(1-cyclohexyl-1_H-tetrazol-5-yl) butoxy]-3,4-dihydro-2-(1_H)-quinolinone for Neurovascular Unit using iTRAQ

Technology

Ahmad Faried, MD., PhD1,2,3_{; Muhammad Z. Arifin, MD}1_{; Agung B. Sutiono,}

MD., PhD1 _{; Hideaki Imai, MD., PhD}2,3_{; Nobuhito Saito, MD., PhD}3

Authors Affiliation:

1_{Department of Neurosurgery, Padjadjaran University, Faculty of Medicine,}

Hasan Sadikin General Hospital, Bandung, Indonesia; 2_{Department of}

Neurosurgery Graduate School of Medicine, Gunma University, Maebashi, Japan; 3_{Department of Neurosurgery, The University of Tokyo, Japan}

Abstract

Object. Quantification proteomic techniques to evaluate a comprehensive comparison of protein expression changes after cilostazol treatment may help us to advances our understanding of its neuroprotective mechanism in vitro.

Methods. Using iTRAQ (multiplexed relative protein quantitation by mass spectrometry), we reported a comparative proteomics profiling of primary mouse brain microvessel endothelial cells (BMVECs) treated with or without cilostazol as a unique features of antiplatelet agent. The significant of these findings was further assessed by Western blot analyses.

Results. Platelet aggregation-, thrombosis-, vasodilator-related proteins as well as enzymes and signaling pathways associated with primary mouse BMVECs injury were found to be differentially expressed on these two differentially-treated BMVECs.

Conclusions. The differential proteins profiling in primary mouse BMVECs treated with or without cilostazol established in our recent study should be valuable for its further exploration in the clinical-setting.