Characterization of Endothelial Cells Associated with Cerebral Arteriovenous Malformation
Authors Jia YC, Fu JY, Huang P, Zhang ZP, Chao B, Bai J
Received 4 February 2020
Accepted for publication 31 March 2020
Published 20 April 2020 Volume 2020:16 Pages 1015—1022
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Yuping Ning
Yu-Chen Jia,1,* Jia-Yue Fu,2,* Ping Huang,3 Zhan-Pu Zhang,3 Bo Chao,3 Jie Bai3
1Inner Mongolia Key Laboratory of Molecular Biology, School of Basic Medical Sciences, Inner Mongolia Medical University, Hohhot, People’s Republic of China; 2Inner Mongolia Medical University, Hohhot, People’s Republic of China; 3Department of Neurosurgery, Affiliated Hospital, Inner Mongolia Medical University, Hohhot, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Jie Bai
Department of Neurosurgery, Affiliated Hospital, Inner Mongolia Medical University, No. 1 Tongdao North Road, Hohhot City, Inner Mongolia 010000, People’s Republic of China
Introduction: Cerebral arteriovenous malformation (cAVM) is a disease characterized by the angiogenesis and remodeling of veins. However, whether vascular endothelial cells (ECs) exhibit morphological and functional changes during cAVM remains unclear. This study aimed to investigate the role of ECs in the pathogenesis of cAVM.
Methods: Rat model of cAVM was established by anastomosing the common carotid artery with the external jugular vein. The digital subtraction angiography (DSA), HE, Masson and immunohistochemical staining were performed to evaluate the model. ECs were isolated from AVM rat model or control rats, and characterized by MTT, cell scratch, and tube formation assays. The secretion of vascular endothelial growth factor (VEGF) was detected by ELISA.
Results: AVM rat model showed typical pathological characteristics of cAVM. In addition, the proliferation, migration and tube formation abilities of ECs of arterialized vein (AV-ECs) were significantly better than those of ECs of normal vein (NV-ECs). Moreover, the levels of secreted VEGF were significantly higher in AV-ECs than in NV-ECs.
Conclusion: AV-ECs isolated from AVM rat model showed increased proliferation, migration and angiogenesis and may be potential target for the treatment of cAVM.
Keywords: cerebral arteriovenous malformation, endothelial cell, angiogenesis, VEGF
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