Astrocytes and oligodendrocytes express different STOP protein isoforms

J Neurosci Res. 2004 Nov 1;78(3):329-37. doi: 10.1002/jnr.20260.

Abstract

Many cell types contain subpopulations of microtubules that resist depolymerizing conditions, such as exposure to cold or to the drug nocodazole. This stabilization is due mainly to polymer association with STOP proteins. In mouse, neurons express two major variants of these proteins, N-STOP and E-STOP (120 kDa and 79 kDa, respectively), whereas fibroblasts express F-STOP (42 kDa) and two minor variants of 48 and 89 kDa. N- and E-STOP induce microtubule resistance to both cold and nocodazole exposure, whereas F-STOP confers microtubule stability only to the cold. Here, we investigated the expression of STOP proteins in oligodendrocytes and astrocytes in culture. We found that STOP proteins were expressed in precursor cells, in immature and mature oligodendrocytes, and in astrocytes. We found that oligodendrocytes express a major STOP variant of 89 kDa, which we called O-STOP, and two minor variants of 42 and 48 kDa. The STOP variants expressed by oligodendrocytes induce microtubule resistance to the cold and to nocodazole. For astrocytes, we found the expression of two STOP variants of 42 and 48 kDa and a new STOP isoform of 60 kDa, which we called A-STOP. The STOP variants expressed by astrocytes induce microtubule resistance to the cold but not to nocodazole, as fibroblast variants. In conclusion, astrocytes and oligodendrocytes express different isoforms of STOP protein, which show different microtubule-stabilizing capacities.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Newborn
  • Astrocytes / drug effects
  • Astrocytes / metabolism*
  • Astrocytes / radiation effects
  • Biomarkers / metabolism
  • Blotting, Western / methods
  • Brain / cytology
  • Brain / metabolism
  • Cells, Cultured
  • Cold Temperature
  • DNA-Binding Proteins / metabolism
  • Gene Expression Regulation / drug effects
  • Gene Expression Regulation / physiology*
  • Glial Fibrillary Acidic Protein / metabolism
  • Immunohistochemistry / methods
  • Mice
  • Microtubule-Associated Proteins / classification
  • Microtubule-Associated Proteins / metabolism*
  • Microtubules / physiology
  • NIH 3T3 Cells / metabolism
  • Nocodazole / pharmacology
  • O Antigens / metabolism
  • Oligodendroglia / drug effects
  • Oligodendroglia / metabolism*
  • Oligodendroglia / radiation effects
  • Protein Isoforms / metabolism*
  • Protein Structure, Tertiary
  • Repressor Proteins / metabolism

Substances

  • Biomarkers
  • DNA-Binding Proteins
  • Glial Fibrillary Acidic Protein
  • Microtubule-Associated Proteins
  • Mtap6 protein, mouse
  • O Antigens
  • Protein Isoforms
  • Repressor Proteins
  • Vps72 protein, mouse
  • Nocodazole