The expression of tenascin-C in neural stem/progenitor cells is stimulated by the growth factors EGF and FGF-2, but not by TGFβ1.
Ursula TheocharidisLars RollAndreas FaissnerPublished in: Cell and tissue research (2021)
Neural stem/progenitor cells (NSPCs) rely on internal and external cues determining their lineage decisions during brain development. The progenitor cells of the embryonic mammalian forebrain reside in the ventricular and subventricular zones of the lateral ventricles, where they proliferate, generate neurons and glial cells, and respond to external cues like growth factors. The extracellular matrix (ECM) surrounds NSPCs and influences the cell fate by providing mechanical scaffold, trophic support, and instructive signals. The ECM molecule tenascin-C (Tnc) is expressed in the proliferative zones of the developing forebrain and involved in the proliferation and maturation of NSPCs. Here, we analyzed the regulation of the Tnc gene expression by NSPCs cultivated under the influence of different growth factors. We observed that the epidermal growth factor (EGF) and the fibroblast growth factor (FGF)-2 strongly increased the expression of Tnc, whereas the transforming growth factor (TGF)β 1 had no effect on Tnc gene expression, in contrast to previous findings in cell cultures of neural and non-neural origin. The stimulation of the Tnc gene expression induced by EGF or FGF-2 was reversible and seen in constantly treated as well as short term stimulated NSPC cultures. The activation depended on the presence of the respective receptors, which was slightly different in cortical and striatal NSPC cultures. Our results confirm the influence of extracellular stimuli regulating the expression of factors that form a niche for NSPCs during embryonic forebrain development.
Keyphrases
- growth factor
- gene expression
- transforming growth factor
- extracellular matrix
- poor prognosis
- dna methylation
- cell fate
- epithelial mesenchymal transition
- single cell
- heart failure
- functional connectivity
- induced apoptosis
- magnetic resonance
- signaling pathway
- resting state
- cell cycle arrest
- spinal cord injury
- stem cells
- bone marrow
- mesenchymal stem cells
- contrast enhanced
- endoplasmic reticulum stress
- magnetic resonance imaging
- cell death
- pi k akt