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Development/Plasticity/Repair

The Growth Arrest-Specific Gene Product Gas6 Promotes the Survival of Human Oligodendrocytes via a Phosphatidylinositol 3-Kinase-Dependent Pathway

Sai Latha Shankar, Kathleen O'Guin, Michael Cammer, F. Arthur McMorris, Trevor N. Stitt, Ross S. Basch, Brian Varnum and Bridget Shafit-Zagardo
Journal of Neuroscience 15 May 2003, 23 (10) 4208-4218; DOI: https://doi.org/10.1523/JNEUROSCI.23-10-04208.2003
Sai Latha Shankar
1Department of Pathology, Albert Einstein College of Medicine, Bronx, New York 10461
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Kathleen O'Guin
1Department of Pathology, Albert Einstein College of Medicine, Bronx, New York 10461
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Michael Cammer
2Department of Analytical Imaging Facility, Albert Einstein College of Medicine, Bronx, New York 10461
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F. Arthur McMorris
3The Wistar Institute, Philadelphia, Pennsylvania 19104
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Trevor N. Stitt
4Regeneron Pharmaceuticals, Tarrytown, New York 10591
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Ross S. Basch
5Department of Pathology, New York University School of Medicine, New York, New York 10016
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Brian Varnum
6Amgen Corporation, Thousand Oaks, California 91320
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Bridget Shafit-Zagardo
1Department of Pathology, Albert Einstein College of Medicine, Bronx, New York 10461
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Abstract

Microarray analysis revealed that transcripts for the Axl and Mer receptor tyrosine kinases are expressed at high levels in O4+-immunopanned oligodendrocytes isolated from second trimester human fetal spinal cord. In humans the sole known ligand for the Axl/Rse/Mer kinases is growth arrest-specific gene 6 (Gas6), which in the CNS is secreted by neurons and endothelial cells. We hypothesized that Gas6 is a survival factor for oligodendrocytes and receptor activation signals downstream to the phosphatidylinositol 3 (PI3)-kinase/Akt pathway to increase cell survival in the absence of cell proliferation. To test this hypothesis, we grew enriched human oligodendrocytes for 6 d on a monolayer of NIH3T3 cells stably expressing Gas6. CNP+ oligodendrocytes on Gas6-secreting 3T3 cells had more primary processes and arborizations than those plated solely on 3T3 cells. Also, a twofold increase in CNP+ and MBP+ oligodendrocytes was observed when they were plated on the Gas6-secreting cells. The effect was abolished in the presence of Axl-Fc but remained unchanged in the presence of the irrelevant receptor fusion molecule TrkA-Fc. A significant decrease in CNP+/TUNEL+ oligodendrocytes was observed when recombinant human Gas6 (rhGas6) was administered to oligodendrocytes plated on poly-l-lysine, supporting a role for Gas6 signaling in oligodendrocyte survival during a period of active myelination in human fetal spinal cord development. PI3-kinase inhibitors blocked the anti-apoptotic effect of rhGas6, whereas a MEK/ERK inhibitor had no effect. Thus Gas6 sustains human fetal oligodendrocyte viability by receptor activation and downstream signaling via the PI3-kinase/Akt pathway.

  • Gas6
  • oligodendrocytes
  • human spinal cord
  • apoptosis
  • tyrosine kinase receptors
  • Axl/Rse/Mer
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The Journal of Neuroscience: 23 (10)
Journal of Neuroscience
Vol. 23, Issue 10
15 May 2003
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The Growth Arrest-Specific Gene Product Gas6 Promotes the Survival of Human Oligodendrocytes via a Phosphatidylinositol 3-Kinase-Dependent Pathway
Sai Latha Shankar, Kathleen O'Guin, Michael Cammer, F. Arthur McMorris, Trevor N. Stitt, Ross S. Basch, Brian Varnum, Bridget Shafit-Zagardo
Journal of Neuroscience 15 May 2003, 23 (10) 4208-4218; DOI: 10.1523/JNEUROSCI.23-10-04208.2003

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The Growth Arrest-Specific Gene Product Gas6 Promotes the Survival of Human Oligodendrocytes via a Phosphatidylinositol 3-Kinase-Dependent Pathway
Sai Latha Shankar, Kathleen O'Guin, Michael Cammer, F. Arthur McMorris, Trevor N. Stitt, Ross S. Basch, Brian Varnum, Bridget Shafit-Zagardo
Journal of Neuroscience 15 May 2003, 23 (10) 4208-4218; DOI: 10.1523/JNEUROSCI.23-10-04208.2003
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Keywords

  • Gas6
  • oligodendrocytes
  • human spinal cord
  • apoptosis
  • tyrosine kinase receptors
  • Axl/Rse/Mer

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