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Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
10:21

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Published on: February 21, 2018

GD1a modulates GM-CSF-induced cell proliferation.

A X S Santos1, J E Maia, P M Crespo

  • 1Laboratório de Bioquímica e Biologia Celular de Lipídios, Depto Bioquímica, ICBS, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil. alinexss@gmail.com

Cytokine
|September 21, 2011
PubMed
Summary

Ganglioside GD1a enhances granulocyte-macrophage colony-stimulating factor (GM-CSF)-induced proliferation in myeloid cells. This suggests GD1a

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In Vitro Differentiation of Mouse Granulocyte-macrophage-colony-stimulating Factor (GM-CSF)-producing T Helper (THGM) Cells
10:27

In Vitro Differentiation of Mouse Granulocyte-macrophage-colony-stimulating Factor (GM-CSF)-producing T Helper (THGM) Cells

Published on: September 10, 2018

Area of Science:

  • Hematology
  • Cell Biology
  • Immunology

Background:

  • Gangliosides are implicated in cell proliferation and differentiation, particularly in hematopoietic cells.
  • Previous studies showed gangliosides support myeloid precursor cell proliferation.
  • Stromal cells shed gangliosides, which are incorporated into myeloid cell membranes.

Purpose of the Study:

  • To investigate the effect of gangliosides on granulocyte-macrophage colony-stimulating factor (GM-CSF)-induced proliferation.
  • To explore the role of ganglioside GD1a in myeloid cell proliferation.

Main Methods:

  • Utilized the monocytic FDC-P1 cell line, dependent on GM-CSF.
  • Cultured cells with GM-CSF and exogenous gangliosides (GM3, GD1a, GM1) or with a ceramide-synthase inhibitor (D-PDMP).
  • Assessed proliferation, GM-CSF receptor alpha (GMRα) expression, C/EBPα levels, and GD1a/GMR co-localization via immunocytochemistry.

Main Results:

  • Exogenous GD1a significantly enhanced GM-CSF-induced proliferation of FDC-P1 cells.
  • Observed increased expression of GMRα and the transcription factor C/EBPα with GD1a addition.
  • Inhibition of endogenous ganglioside synthesis reduced proliferation, which was restored by exogenous GD1a.
  • Demonstrated co-localization of GD1a and GMR.

Conclusions:

  • Ganglioside GD1a modulates GM-CSF-mediated proliferative responses.
  • GD1a's role in hematopoiesis is significant.
  • Potential implications in immunology, Alzheimer disease, alveolar proteinosis, and other GM-CSF-related processes.