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Title: Activation of Wnt3α/β-catenin signal pathway attenuates apoptosis of the cerebral microvascular endothelial cells induced by oxygen-glucose deprivation

Abstract

Brain microvascular endothelial cells (BMECs) play vital roles in cerebral ischemia, during which many signal pathways mediate BMECs apoptosis. In this study, we explored the potential role of Wnt3α/β-catenin signal in BMECs apoptosis induced by ischemia. Here, we found that oxygen-glucose deprivation (OGD) could induce apoptosis of BMECs with Wnt3a mRNA expression decrease. Meanwhile, activation Wnt3a/β-catenin signal with exogenous Wnt3α protein (100 ng/ml) or Lithium Chloride (LiCl, 4 mM) decreased significantly apoptosis of BMECs induced by OGD with increasing expression of Bcl-2 in the whole cell and β-catenin in the nucleus. But, inhibition Wnt3a/β-catenin signal with DKK1 (100 ng/ml) or 2.4-diamino quinazoline (DQ, 0.2 μM) increased apoptosis of BMECs with decreasing expression of Bcl-2. These results suggest that activation Wnt3α/β-catenin signal attenuate apoptosis of BMECs induced by ischemia. - Highlights: • OGD induced BMECs apoptosis with Wnt3a mRNA expression decrease. • Activation Wnt signal reduced BMECs apoptosis with increasing Bcl-2 and β-catenin. • Inhibition Wnt signal increased BMECs apoptosis with decreasing Bcl-2. • Wnt3α/β-catenin signal attenuates apoptosis of BMECs induced by ischemia.

Authors:
 [1];  [2];  [3];  [1];  [2]; ;  [1];  [2];  [1]
  1. Institute of Neurobiology, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi 710061 (China)
  2. (China)
  3. Department of Human Anatomy, Xi'an Medical University, Xi'an, Shaanxi 710021 (China)
Publication Date:
OSTI Identifier:
22719028
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 490; Journal Issue: 2; Other Information: Copyright (c) 2017 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; APOPTOSIS; BLOOD; BLOOD-BRAIN BARRIER; BORON CHLORIDES; BRAIN; GLUCOSE; GLYCOGEN; INHIBITION; ISCHEMIA; LITHIUM; LITHIUM CHLORIDES; MESSENGER-RNA; PHOSPHOTRANSFERASES

Citation Formats

Zhang, Jianshui, Department of Human Anatomy, Histology and Embryology, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi 710061, Zhang, Junfeng, Qi, Cunfang, Department of Human Anatomy, Qinghai University School of Medicine, Xining, Qinghai 810001, Yang, Pengbo, Chen, Xinlin, Department of Human Anatomy, Histology and Embryology, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi 710061, and Liu, Yong. Activation of Wnt3α/β-catenin signal pathway attenuates apoptosis of the cerebral microvascular endothelial cells induced by oxygen-glucose deprivation. United States: N. p., 2017. Web. doi:10.1016/J.BBRC.2017.03.130.
Zhang, Jianshui, Department of Human Anatomy, Histology and Embryology, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi 710061, Zhang, Junfeng, Qi, Cunfang, Department of Human Anatomy, Qinghai University School of Medicine, Xining, Qinghai 810001, Yang, Pengbo, Chen, Xinlin, Department of Human Anatomy, Histology and Embryology, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi 710061, & Liu, Yong. Activation of Wnt3α/β-catenin signal pathway attenuates apoptosis of the cerebral microvascular endothelial cells induced by oxygen-glucose deprivation. United States. doi:10.1016/J.BBRC.2017.03.130.
Zhang, Jianshui, Department of Human Anatomy, Histology and Embryology, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi 710061, Zhang, Junfeng, Qi, Cunfang, Department of Human Anatomy, Qinghai University School of Medicine, Xining, Qinghai 810001, Yang, Pengbo, Chen, Xinlin, Department of Human Anatomy, Histology and Embryology, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi 710061, and Liu, Yong. Sat . "Activation of Wnt3α/β-catenin signal pathway attenuates apoptosis of the cerebral microvascular endothelial cells induced by oxygen-glucose deprivation". United States. doi:10.1016/J.BBRC.2017.03.130.
@article{osti_22719028,
title = {Activation of Wnt3α/β-catenin signal pathway attenuates apoptosis of the cerebral microvascular endothelial cells induced by oxygen-glucose deprivation},
author = {Zhang, Jianshui and Department of Human Anatomy, Histology and Embryology, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi 710061 and Zhang, Junfeng and Qi, Cunfang and Department of Human Anatomy, Qinghai University School of Medicine, Xining, Qinghai 810001 and Yang, Pengbo and Chen, Xinlin and Department of Human Anatomy, Histology and Embryology, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi 710061 and Liu, Yong},
abstractNote = {Brain microvascular endothelial cells (BMECs) play vital roles in cerebral ischemia, during which many signal pathways mediate BMECs apoptosis. In this study, we explored the potential role of Wnt3α/β-catenin signal in BMECs apoptosis induced by ischemia. Here, we found that oxygen-glucose deprivation (OGD) could induce apoptosis of BMECs with Wnt3a mRNA expression decrease. Meanwhile, activation Wnt3a/β-catenin signal with exogenous Wnt3α protein (100 ng/ml) or Lithium Chloride (LiCl, 4 mM) decreased significantly apoptosis of BMECs induced by OGD with increasing expression of Bcl-2 in the whole cell and β-catenin in the nucleus. But, inhibition Wnt3a/β-catenin signal with DKK1 (100 ng/ml) or 2.4-diamino quinazoline (DQ, 0.2 μM) increased apoptosis of BMECs with decreasing expression of Bcl-2. These results suggest that activation Wnt3α/β-catenin signal attenuate apoptosis of BMECs induced by ischemia. - Highlights: • OGD induced BMECs apoptosis with Wnt3a mRNA expression decrease. • Activation Wnt signal reduced BMECs apoptosis with increasing Bcl-2 and β-catenin. • Inhibition Wnt signal increased BMECs apoptosis with decreasing Bcl-2. • Wnt3α/β-catenin signal attenuates apoptosis of BMECs induced by ischemia.},
doi = {10.1016/J.BBRC.2017.03.130},
journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 2,
volume = 490,
place = {United States},
year = {2017},
month = {8}
}