论文已发表
注册即可获取德孚的最新动态
IF 收录期刊
Authors Si M, Jiao X, Li Y, Chen H, He P, Jiang F
Received 23 September 2017
Accepted for publication 28 November 2017
Published 12 February 2018 Volume 2018:10 Pages 305—313
DOI https://doi.org/10.2147/CMAR.S152419
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Akshita Wason
Peer reviewer comments 3
Editor who approved publication: Dr Antonella D'Anneo
Aim: Central nervous system (CNS)
metastasis is a major obstacle in the treatment of leukemia, and the underlying
mechanisms of leukemia CNS metastasis are not fully understood. The present
study is an investigation of the role of the CNS microenvironment in leukemia
CNS metastasis.
Methods: Analog blood–brain barrier (BBB) was set by coculturing
human brain microvascular endothelial cells (HBMVECs) and leukemia cells (U937
and IL-60), as well as HBMVECs and sera from leukemia patients, in vitro. The
permeability of the HBMVEC monolayer and the levels of tight junction proteins,
cytokines and chemokines (C&Ckines) were measured.
Results: The permeability of HBMVECs increased when
cocultured with leukemia sera. The expression of C&Ckines was significantly
upregulated in HBMVECs cocultured with leukemia sera or leukemia cells,
compared to the normal sera (P <0.05,
respectively). Specifically, significantly higher levels of vascular
endothelial growth factor A (VEGF-A) and matrix metalloprotease 9 (MMP-9) were
found in HBMVECs and leukemia cells/sera coculturing systems.
Conclusion: Both leukemia cells and the molecules in
leukemia sera play an important role in leukemia CNS metastasis. VEGF-A and
MMPs may be the main factors resulting in the degradation of the BBB and
inducing the CNS migration of leukemia cells.
Keywords: CNS leukemia,
cytokine, chemokine, U937, IL-60