Type II glucocorticoid receptors are expressed in oligodendrocytes and astrocytes.
Glucocorticoid hormones affect gene expression directly at the level of transcription via intracellular receptors that translocate to the nucleus in the presence of steroid. In the brain, two types of high-affinity receptors bind glucocorticoids, the type I, mineralocorticoid receptor and the type II, glucocorticoid receptor (GR). Both receptor types are expressed by many types of neurons. Although binding studies have suggested that glial cells may also express receptors, the expression of these receptors in specific classes of glia has not been studied previously. This immunocytochemical study was undertaken to determine which of the different classes of glial cells express type II GR. Primary cultures of mixed glial cells from rat cerebrum and cerebellum, purified oligodendrocytes and astrocytes, as well as two glial tumor cell lines were screened for the expression of glucocorticoid receptors using a mouse monoclonal antibody directed against rat liver GR (BuGR-2). Glial cell types were identified by morphology and immunoreactivity (IR) with antibodies directed against glial fibrillary acidic protein (GFAP), cyclic nucleotide phosphodiesterase (CNP), or myelin basic protein (MBP). Double immunofluorescence microscopy revealed that all GFAP-IR cells (type 1 and type 2 astrocytes), all CNP- or MBP-IR cells (oligodendrocytes), as well as immature and intermediate cell types expressed GR, although at different levels. C6 glioma and JScl1 Schwannoma cells were observed to express moderate to high levels of GR. Furthermore, cells grown in the absence of glucocorticoids had diffuse GR staining over the cytoplasm, whereas cells grown in the presence of the synthetic glucocorticoid dexamethasone had strong nuclear staining. These results demonstrate that, in vitro, all classes of glial cells express glucocorticoid receptors that can translocate to the nucleus in the presence of hormone. These observations suggest that glial cells are major targets for glucocorticoid-directed control of gene transcription in the nervous system.
Vielkind
U
U
Department of Neurobiology, Rochester University School of Medicine, New York.
Walencewicz
A
A
Levine
J M
JM
Bohn
M C
MC
D001253:Astrocytes / Q000378:metabolism*; D002478:Cells, Cultured; D002531:Cerebellum / Q000166:cytology; D002540:Cerebral Cortex / Q000166:cytology; D003907:Dexamethasone / Q000494:pharmacology; D005786:Gene Expression Regulation; D005910:Glioma / Q000473:pathology; D009363:Neoplasm Proteins / Q000096:biosynthesis; D009442:Neurilemmoma / Q000473:pathology; D009836:Oligodendroglia / Q000378:metabolism*; D011499:Protein Processing, Post-Translational / Q000187:drug effects; D011965:Receptors, Glucocorticoid / Q000096:biosynthesis*; D014407:Tumor Cells, Cultured / Q000378:metabolism
D009363:Neoplasm Proteins; D011965:Receptors, Glucocorticoid; C028697:dexamethasone receptor; D003907:Dexamethasone