Han Yan1, Xiaolong Zhu1, Junchao Xie1, Yanxin Zhao2, Xueyuan Liu3. 1. Department of Neurology, Shanghai Tenth People's Hospital, Tongji University, School of Medicine, 301 Middle Yanchang Road, Shanghai 200072, PR China. 2. Department of Neurology, Shanghai Tenth People's Hospital, Tongji University, School of Medicine, 301 Middle Yanchang Road, Shanghai 200072, PR China. Electronic address: zhao_yanxin@126.com. 3. Department of Neurology, Shanghai Tenth People's Hospital, Tongji University, School of Medicine, 301 Middle Yanchang Road, Shanghai 200072, PR China. Electronic address: liuxy@tongji.edu.cn.
Abstract
OBJECTIVE: This study aimed to investigate whether β-amyloid (Aβ) was able to enhance neurocan expression in a Sox9 dependent manner in astrocytes. METHODS AND MATERIALS: Astrocytes were incubated with Aβ at different concentrations, the expression of Sox9 and neurocan was detected by Western blot assay. Meanwhile, the viability and proliferation of astrocytes were assessed by MTT assay. Then, the Sox9 expression was silenced, and the expression of Sox9 and neurocan was examined. RESULTS: After incubation with Aβ, the viability of astrocytes was increased regardless silencing of Sox9 (all P<0.05). The proliferation of astrocytes was also gradually increased with the increase in the time of Aβ incubation (all P<0.05). With the increase in Aβ concentration, the expression of Sox9 and neurocan was also increased (all P<0.05). However, after silencing of Sox9 expression, the neurocan expression was significantly reduced as compared to control group and scra-siRNA group (all P<0.05). CONCLUSION: Our study shows the viability and proliferation of astrocytes are significantly increased by Aβ in a dose dependent manner. Moreover, Aβ may effectively up-regulate the neurocan expression via regulating Sox9.
OBJECTIVE: This study aimed to investigate whether β-amyloid (Aβ) was able to enhance neurocan expression in a Sox9 dependent manner in astrocytes. METHODS AND MATERIALS: Astrocytes were incubated with Aβ at different concentrations, the expression of Sox9 and neurocan was detected by Western blot assay. Meanwhile, the viability and proliferation of astrocytes were assessed by MTT assay. Then, the Sox9 expression was silenced, and the expression of Sox9 and neurocan was examined. RESULTS: After incubation with Aβ, the viability of astrocytes was increased regardless silencing of Sox9 (all P<0.05). The proliferation of astrocytes was also gradually increased with the increase in the time of Aβ incubation (all P<0.05). With the increase in Aβ concentration, the expression of Sox9 and neurocan was also increased (all P<0.05). However, after silencing of Sox9 expression, the neurocan expression was significantly reduced as compared to control group and scra-siRNA group (all P<0.05). CONCLUSION: Our study shows the viability and proliferation of astrocytes are significantly increased by Aβ in a dose dependent manner. Moreover, Aβ may effectively up-regulate the neurocan expression via regulating Sox9.
Authors: Isabelle A Birt; Megan H Hagenauer; Sarah M Clinton; Cigdem Aydin; Peter Blandino; John D H Stead; Kathryn L Hilde; Fan Meng; Robert C Thompson; Huzefa Khalil; Alex Stefanov; Pamela Maras; Zhifeng Zhou; Elaine K Hebda-Bauer; David Goldman; Stanley J Watson; Huda Akil Journal: Biol Psychiatry Date: 2020-05-27 Impact factor: 13.382
Authors: Do Yeon Lee; Chul Ju Hwang; Ji Yeon Choi; Mi Hee Park; Min Ji Song; Ki Wan Oh; Sang Bae Han; Woo Kyu Park; Hee Yeong Cho; Sung Yun Cho; Hye Byn Park; Min Jong Song; Jin Tae Hong Journal: Oncotarget Date: 2017-08-02
Authors: Flora H Duits; Gunnar Brinkmalm; Charlotte E Teunissen; Ann Brinkmalm; Philip Scheltens; Wiesje M Van der Flier; Henrik Zetterberg; Kaj Blennow Journal: Alzheimers Res Ther Date: 2018-01-15 Impact factor: 6.982