Abstract
Myelin oligodendrocyte glycoprotein (MOG) is a central nervous system myelin-specific molecule expressed on the outer lamellae of myelin. To date, the exact function of MOG has remained unknown, with MOG knockout mice displaying normal myelin ultrastructure and no apparent specific phenotype. In this paper, we identify nerve growth factor (NGF) as a binding partner for MOG and demonstrate that this interaction is capable of sequestering NGF from TrkA-expressing neurons to modulate axon growth and survival. Deletion of MOG results in aberrant sprouting of nociceptive neurons in the spinal cord. Binding of NGF to MOG may offer widespread implications into mechanisms that underlie pain pathways.
Publication types
-
Research Support, N.I.H., Extramural
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Amino Acid Sequence
-
Animals
-
Axons / metabolism*
-
CHO Cells
-
Cell Survival
-
Coculture Techniques
-
Cricetulus
-
Ganglia, Spinal / metabolism*
-
Ganglia, Spinal / pathology
-
Genotype
-
Mice, Knockout
-
Molecular Sequence Data
-
Myelin-Oligodendrocyte Glycoprotein / deficiency
-
Myelin-Oligodendrocyte Glycoprotein / genetics
-
Myelin-Oligodendrocyte Glycoprotein / metabolism*
-
Nerve Growth Factor / metabolism*
-
Oligodendroglia / metabolism*
-
Phenotype
-
Protein Binding
-
Rats, Sprague-Dawley
-
Receptor, trkA / metabolism
-
Signal Transduction
-
Spinal Cord / metabolism*
-
Spinal Cord / pathology
-
Transfection
Substances
-
Mog protein, mouse
-
Mog protein, rat
-
Myelin-Oligodendrocyte Glycoprotein
-
Nerve Growth Factor
-
Receptor, trkA