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Neutral glycolipid and ganglioside composition of type‐1 and type‐2 astrocytes from rat cerebral hemisphere
Author(s) -
Murakami K.,
Asou H.,
Adachi T.,
Takagi T.,
Kunimoto M.,
Saito H.,
Uyemura K.
Publication year - 1999
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19990201)55:3<382::aid-jnr13>3.0.co;2-m
Subject(s) - ganglioside , glycolipid , composition (language) , chemistry , neuroscience , biochemistry , biology , art , literature
We reported previously that the major gangliosides in primary mixed‐type astrocyte cultures are GM 3 and GD 3 . To obtain more information regarding the exact distribution of glycosphingolipids in different types of astrocytes, we established a line of type‐1 astrocytes that are characterized by a Ran‐2 positive, broad flat morphology, and by the absence of binding to A2B5 antibodies. We also purified O‐2A progenitor cells by immunopanning and cultured them in the presence of 10% newborn calf serum. They differentiated into type‐2 astrocytes that were identified by immunostaining for each of GD 3 , A2B5, and GFAP. Using these cell cultures, we demonstrate that the major gangliosides were GM 3 in type‐1 astrocytes and GM 3 and GD 3 in type‐2 astrocytes. In addition, a set of neutral glycolipids was identified based on the HP‐TLC migration properties of CMH, CDH, CTH, and Glob, but the component distribution of these glycolipids is related to that of glycolipids of astrocytes. A marked increase in the expression of CTH and Glob was shown in type‐2 astrocytes. The amount of neutral glycolipid‐sugar was higher in the type‐2 astrocytes than in the type‐1 astrocytes. These results suggest that the increase in the total glycosphingolipid content and the change in the neutral glycolipid composition produced by type‐2 astrocytes may be related to their biological functions and the cellular compositions. J. Neurosci. Res. 55:382–393, 1999. © 1999 Wiley‐Liss, Inc.