2. Academic Validation
  3. Suppression of Nestin reveals a critical role for p38-EGFR pathway in neural progenitor cell proliferation

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

  • Oncotarget. 2016 Dec 27;7(52):87052-87063. doi: 10.18632/oncotarget.13498.
Wentao Hu 1,  Hong Lu 1,  Shang Wang 1,  Wenhan Yin 1,  Xujie Liu 2 3 4 5 6,  Lin Dong 7,  Richard Chiu 8,  Li Shen 7,  Wen-Jing Lu 2 3 4 5,  Feng Lan 2 3 4 5
Affiliations

Affiliations

  • 1 Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
  • 2 Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, China.
  • 3 Beijing Lab for Cardiovascular Precision Medicine, Capital Medical University, Beijing, China.
  • 4 The Key Laboratory of Remodeling-Related Cardiovascular Disease, Ministry of Education, Beijing, China.
  • 5 Beijing Collaborative Innovation Center for Cardiovascular Disorders, Anzhen Hospital, Capital Medical University, Beijing, China.
  • 6 Deparment of Radiological Medicine, Chongqing Medical University, Chongqing, China.
  • 7 Department of Cell Biology Peking University Health Science Center, Beijing, China.
  • 8 Deparment of Radiology, Stanford University School of Medicine, Stanford, California, USA.
PMID: 27894083 DOI: 10.18632/oncotarget.13498
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.

Keywords

EGFR; NPCs; nestin; proliferation; self-renewal.

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