Oncotarget

Research Papers:

Suppression of Nestin reveals a critical role for p38-EGFR pathway in neural progenitor cell proliferation

Wentao Hu _, Hong Lu, Shang Wang, Wenhan Yin, Xujie Liu, Lin Dong, Richard Chiu, Li Shen, Wen-Jing Lu and Feng Lan

PDF  |  HTML  |  Supplementary Files  |  How to cite

Oncotarget. 2016; 7:87052-87063. https://doi.org/10.18632/oncotarget.13498

Metrics: PDF 1225 views  |   HTML 1944 views  |   ?  


Abstract

Wentao Hu1, Hong Lu1, Shang Wang1, Wenhan Yin1, Xujie Liu2,3,4,5,6, Lin Dong7, Richard Chiu8, Li Shen7, Wen-Jing Lu2,3,4,5, Feng Lan2,3,4,5

1Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China

2Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, China

3Beijing Lab for Cardiovascular Precision Medicine, Capital Medical University, Beijing, China

4The Key Laboratory of Remodeling-Related Cardiovascular Disease, Ministry of Education, Beijing, China

5Beijing Collaborative Innovation Center for Cardiovascular Disorders, Anzhen Hospital, Capital Medical University, Beijing, China

6Deparment of Radiological Medicine, Chongqing Medical University, Chongqing, China

7Department of Cell Biology Peking University Health Science Center, Beijing, China

8Deparment of Radiology, Stanford University School of Medicine, Stanford, California, USA

Correspondence to:

Feng Lan, email: [email protected]

Wen-Jing Lu, email: [email protected]

Keywords: nestin, NPCs, proliferation, EGFR, self-renewal

Received: July 27, 2016     Accepted: October 14, 2016     Published: November 22, 2016

ABSTRACT

The expression of intermediate filament Nestin is necessary for the neural progenitor cells (NPCs) to maintain stemness, but the underlying cellular and molecular mechanism remains unclear. In this study, we demonstrated that Nestin is required for the self-renew of NPCs through activating MAPK and EGFR pathways. Knockdown of Nestin by shRNA inhibited cell cycle progression and proliferation in mouse NPCs. Moreover, suppression of Nestin reduced expression of the epidermal growth factor receptor (EGFR) in NPCs and inhibited the mitogenic effects of EGF on these cells. Treatment of NPCs with p38-MAPK inhibitor PD169316 reversed cell cycle arrest caused by the knockdown of Nestin. Our findings indicate that Nestin promotes NPC proliferation via p38-MAPK and EGFR pathways, and reveals the necessity of these pathways in NPCs self-renewal.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.
PII: 13498