scholarly journals Influence of Dopamine on Precursor Cell Proliferation and Differentiation in the Embryonic Mouse Telencephalon

2004 ◽  
Vol 26 (2-4) ◽  
pp. 229-244 ◽  
Author(s):  
Margherita Popolo ◽  
Deirdre M. McCarthy ◽  
Pradeep G. Bhide
Keyword(s):  
Cell Proliferation ◽  
Precursor Cell ◽  
Embryonic Mouse ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation

scholarly journals Rac1 modulates mammalian lung branching morphogenesis in part through canonical Wnt signaling

2016 ◽  
Vol 311 (6) ◽  
pp. L1036-L1049 ◽  
Author(s):  
Soula Danopoulos ◽  
Michael Krainock ◽  
Omar Toubat ◽  
Matthew Thornton ◽  
Brendan Grubbs ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Wnt Signaling ◽  
Branching Morphogenesis ◽  
Mouse Lung ◽  
Canonical Wnt Signaling ◽  
Embryonic Mouse ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Canonical Wnt ◽  
Lung Branching

Lung branching morphogenesis relies on a number of factors, including proper epithelial cell proliferation and differentiation, cell polarity, and migration. Rac1, a small Rho GTPase, orchestrates a number of these cellular processes, including cell proliferation and differentiation, cellular alignment, and polarization. Furthermore, Rac1 modulates both noncanonical and canonical Wnt signaling, important pathways in lung branching morphogenesis. Culture of embryonic mouse lung explants in the presence of the Rac1 inhibitor (NSC23766) resulted in a dose-dependent decrease in branching. Increased cell death and BrdU uptake were notably seen in the mesenchyme, while no direct effect on the epithelium was observed. Moreover, vasculogenesis was impaired following Rac1 inhibition as shown by decreased Vegfa expression and impaired LacZ staining in Flk1-Lacz reporter mice. Rac1 inhibition decreased Fgf10 expression in conjunction with many of its associated factors. Moreover, using the reporter lines TOPGAL and Axin2-LacZ, there was an evident decrease in canonical Wnt signaling in the explants treated with the Rac1 inhibitor. Activation of canonical Wnt pathway using WNT3a or WNT7b only partially rescued the branching inhibition. Moreover, these results were validated on human explants, where Rac1 inhibition resulted in impaired branching and decreased AXIN2 and FGFR2b expression. We therefore conclude that Rac1 regulates lung branching morphogenesis, in part through canonical Wnt signaling. However, the exact mechanisms by which Rac1 interacts with canonical Wnt in human and mouse lung requires further investigation.

scholarly journals Normal sulfation levels regulate spinal cord neural precursor cell proliferation and differentiation

2012 ◽  
Vol 7 (1) ◽  
pp. 20 ◽  
Author(s):  
Michael Karus ◽  
Samira Samtleben ◽  
Claudia Busse ◽  
Teresa Tsai ◽  
Irmgard D Dietzel ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Cell Proliferation ◽  
Precursor Cell ◽  
Neural Precursor ◽  
Neural Precursor Cell ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation

scholarly journals A lipophilic iron chelator can replace transferrin as a stimulator of cell proliferation and differentiation.

1984 ◽  
Vol 98 (2) ◽  
pp. 596-601 ◽  
Author(s):  
W Landschulz ◽  
I Thesleff ◽  
P Ekblom
Keyword(s):  
Cell Proliferation ◽  
Iron Chelator ◽  
Normal Serum ◽  
Ferric Ion ◽  
Embryonic Mouse ◽  
Chemically Defined Media ◽  
Defined Media ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Pyridoxal Isonicotinoyl Hydrazone

Of the different growth supplements used in chemically defined media, only transferrin is required for differentiation of tubules in the embryonic mouse metanephros. Since transferrin is an iron-carrying protein, we asked whether iron is crucial for tubulogenesis. Differentiation of metanephric tubules both in whole embryonic kidneys and in a transfilter system was studied. The tissues were grown in chemically defined media containing transferrin, apotransferrin, the metal-chelator complex ferric pyridoxal isonicotinoyl hydrazone (FePIH), and excesses of ferric ion. Although we found that apotransferrin was not as effective as iron-loaded transferrin in promoting proliferation in the differentiating kidneys, excess ferric ion at up to 100 microM, five times the normal serum concentration, could not promote differentiation or proliferation. However, iron coupled to the nonphysiological, lipophilic iron chelator, pyridoxal isonicotinoyl hydrazone, to form FePIH, could sustain levels of cell proliferation and tubulogenesis similar to those attained by transferrin. Thus, the role of transferrin in cell proliferation during tubulogenesis is solely to provide iron. Since FePIH apparently bypasses the receptor-mediated route of iron intake, the use of FePIH as a tool for investigating cell proliferation and its regulation is suggested.

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