1. Academic Validation
  2. Epiregulin promotes the migration and chemotaxis ability of adipose-derived mesenchymal stem cells via mitogen-activated protein kinase signaling pathways

Epiregulin promotes the migration and chemotaxis ability of adipose-derived mesenchymal stem cells via mitogen-activated protein kinase signaling pathways

  • J Cell Biochem. 2018 Nov;119(10):8450-8459. doi: 10.1002/jcb.27069.
Yangyang Cao 1 Liping Wang 1 Haoqing Yang 1 Xiao Lin 1 2 Guoqing Li 1 3 Nannan Han 1 4 Juan Du 1 Zhipeng Fan 1
Affiliations

Affiliations

  • 1 Laboratory of Molecular Signaling and Stem Cells Therapy, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, China.
  • 2 Department of Implant Dentistry, Capital Medical University School of Stomatology, Beijing, China.
  • 3 Molecular Laboratory for Gene Therapy and Tooth Regeneration, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, Beijing, China.
  • 4 Department of Periodontology, Capital Medical University School of Stomatology, Beijing, China.
Abstract

To investigate the function of Epiregulin (EREG) in the migration and chemotaxis ability of mesenchymal stem cells. Adipose-derived stem cells (ADSCs) were used in this investigation. Lentiviral EREG short hairpin RNA was applied to silence EREG expression in ADSCs. Human recombinant EREG protein (rhEREG) was used to perform a gain-of-function study. Scratch-simulated wound migration and transwell chemotaxis assays were used to examine the migration and chemotaxis capacity of ADSCs in vitro. Using a Western blot assay, the expressions of p38 mitogen-activated protein kinase (p38 MAPK), c-Jun N-terminal kinase (JNK), extracellular signal-regulated protein kinases 1 and 2 (ERK1/2), and protein kinase B were detected. Depletion of EREG caused by specific short hairpin RNA restrained the migration and chemotaxis ability of ADSCs and inhibited the expressions of phosphorylated p38 MAPK, JNK, and ERK1/2. rhEREG improved ADSCs migration and chemotaxis capacity, which was repressed by knockdown of EREG and rescued the expressions of phosphorylated p38 MAPK, JNK, and ERK1/2 impaired by silencing EREG. Furthermore, rhEREG-improved migration and chemotaxis ability in EREG-depleted-ADSCs was restricted by a specific inhibitor, SB203580, for blocking p38 MAPK signaling, PD98059 for blocking ERK1/2 signaling, or SP600125 for blocking JNK signaling in ADSCs separately. EREG promotes migration and chemotaxis ability of ADSCs through MAPK signaling pathways.

Keywords

adipose-derived stem cells (ADSCs); chemotaxis; epiregulin (EREG); migration; mitogen-activated protein kinase (MAPK) pathway.

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