The reaction of glial progenitor cells in remyelination following ethidium bromide-induced demyelination in the mouse spinal cord.

Abstract

The present study investigated how glial progenitor cells participated in the process of remyelination following ethidium bromide (EBr)-induced demyelination in the adult mouse spinal cord. In situ hybridization techniques for detecting mRNA for platelet-derived growth factor alpha receptor (PDGFalphaR) and proteolipid protein (PLP) were employed to identify glial progenitor cells and mature oligodendrocytes, respectively. During the demyelination stage and early stage of remyelination, large cells strongly expressing PDGFalphaR mRNA were observed in the border of the demyelinating lesion, and with immunohistochemistry they exhibited positive labeling of the astrocytic marker glial fibrillary acidic protein (GFAP). Other glial progenitor cells expressing PDGFalphaR mRNA proliferated around the lesion during the demyelination stage. During the remyelination stage, some PDGFalphaR mRNA-positive cells partly expressed mRNA for PLP in the periphery of the demyelinating lesion. These results suggest that PDGFalphaR mRNA-positive glial progenitor cells may give rise to both astrocytes and oligodendrocytes, which participate in remyelination following demyelination.

• Authors: Shigeko Fushimi, Teruo Shirabe
• Journal: Neuropathology : official journal of the Japanese Society of Neuropathology (Neuropathology) Vol. 22 Issue 4 Pg. 233-42 (Dec 2002) ISSN: 0919-6544 [Print] Australia
• PMID: 12564762 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Enzyme Inhibitors
• Glial Fibrillary Acidic Protein
• Myelin Proteolipid Protein
• RNA, Messenger
• Receptor, Platelet-Derived Growth Factor alpha
• Ethidium

Topics

• Animals
• Astrocytes (metabolism)
• Cell Differentiation
• Demyelinating Diseases (chemically induced, metabolism, pathology)
• Enzyme Inhibitors (administration & dosage, pharmacology)
• Ethidium (administration & dosage, pharmacology)
• Glial Fibrillary Acidic Protein (metabolism)
• Immunohistochemistry
• In Situ Hybridization
• Injections, Spinal
• Male
• Mice
• Mice, Inbred BALB C
• Myelin Proteolipid Protein (genetics)
• Myelin Sheath (physiology)
• Neuroglia (metabolism)
• Oligodendroglia (metabolism)
• RNA, Messenger (analysis)
• Receptor, Platelet-Derived Growth Factor alpha (genetics)
• Spinal Cord (cytology, metabolism, pathology)
• Stem Cells (metabolism)
• Time Factors