Cadherin-11 Regulates Cell Proliferation via the PDGFR beta-ERK1/2 Signaling Pathway in Human Mesenchymal Stem Cells

F.R. Passanha, M.L. Divinagracia, V.L.S. LaPointe*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Controlling stem cell fate is the cornerstone of regenerative medicine. Cadherins have an important role in cell fate commitment and the function of cadherin-11 in the regulation of differentiation in human mesenchymal stem cells (hMSCs) has recently come to light. To better understand how cadherin-11 regulates hMSC behavior, we explored its interaction with receptor tyrosine kinases (RTK), an important family of proteins involved in a myriad of cellular functions. In this study, we provide evidence that cadherin-11, a cell adhesion protein expressed in hMSCs, regulates the activity of several RTKs, including PDGFR beta and PDGFR alpha. By knocking down cadherin-11 we found that the changes in the RTK activity caused hyperactivation of the MAPK pathways, which were sustained through the phosphorylation and nuclear translocation of ERK1/2 and subsequently caused a decrease in cell proliferation. Together these results provide compelling evidence for the important role of the interaction of cadherin-11 and RTKs in the behavior of hMSCs.
Original languageEnglish
Pages (from-to)165-174
Number of pages10
JournalStem Cells
Volume40
Issue number2
Early online date1 Jan 2022
DOIs
Publication statusPublished - 16 Mar 2022

Keywords

  • adult stem cells
  • cell adhesion molecules
  • cell biology
  • cellular proliferation
  • mesenchymal stem cells (MSCs)
  • proliferation
  • EPIDERMAL-GROWTH-FACTOR
  • STROMAL CELLS
  • RECEPTOR-BETA
  • G1 PHASE
  • ACTIVATION
  • EXPRESSION
  • BINDING

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