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Ca(v)3.2 calcium channels control an autocrine mechanism that promotes neuroblastoma cell differentiation.

Abstract
Calcium influx via low-voltage activated alpha(1H) (Ca(v)3.2) T-currents participates in the morphological and electrical differentiation of neuroblastoma NG108-15 cells. We investigated whether an autocrine mechanism could contribute to this differentiation process. The presence of factors secreted by NG108-15 cells was identified through the use of conditioned media (CM) obtained from differentiated cells. These CM significantly increased neuritogenesis with no change in the HVA calcium channel expression. CM-induced neuritogenesis persists during alpha(1H) current block, whereas CM obtained from cells transfected with an alpha(1H) antisense did not induce neuritogenesis. These data indicate that morphological differentiation of NG108-15 cells depends on an autocrine mechanism, which is controlled by alpha(1H) currents. Such a mechanism is likely to play a role in the various differentiation processes that imply alpha(1H) T-type Ca(2+) channels.
AuthorsJean Chemin, Joël Nargeot, Philippe Lory
JournalNeuroreport (Neuroreport) Vol. 15 Issue 4 Pg. 671-5 (Mar 22 2004) ISSN: 0959-4965 [Print] England
PMID15094473 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • CACNA1H protein, human
  • Calcium Channels, T-Type
  • Culture Media, Conditioned
  • Oligoribonucleotides, Antisense
Topics
  • Animals
  • Autocrine Communication (drug effects, genetics, physiology)
  • Calcium Channels, T-Type (genetics, metabolism)
  • Calcium Signaling (drug effects, genetics, physiology)
  • Cell Differentiation (drug effects, genetics, physiology)
  • Cell Line, Tumor
  • Culture Media, Conditioned (pharmacology)
  • Membrane Potentials (drug effects, genetics)
  • Mice
  • Neurites (drug effects, metabolism)
  • Neuroblastoma (metabolism)
  • Neurons (cytology, drug effects, metabolism)
  • Oligoribonucleotides, Antisense
  • Patch-Clamp Techniques
  • Rats
  • Stem Cells (cytology, drug effects, metabolism)

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