ArticleCellular and molecular neurobiology1995
Dexamethasone induces an increase in intracellular and membrane-associated lipocortin-1 (annexin-1) in rat astrocyte primary cultures.
Article in Cellular and molecular neurobiology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Role of stress-related glucocorticoid changes in astrocyte-oligodendrocyte interactions that regulate myelin production and maintenance.Histology and histopathology · 2023Review
- Effects of glucocorticoids in depression: Role of astrocytes.AIMS neuroscience · 2018Review
- Article
- Responses of glial cells to stress and glucocorticoids.Current immunology reviews · 2010Article
- Pyrimidine nucleotide-stimulated thromboxane A2 release from cultured glia.Cellular and molecular neurobiology · 1998Article
- Expression of annexin II in glioma cell lines and in brain tumor biopsies.Journal of neuro-oncology · 1998Article
- Effect of annexin-1 on experimental autoimmune encephalomyelitis (EAE) in the rat.Clinical and experimental immunology · 1998Article
- Fifteenth Gaddum Memorial Lecture December 1994. Stress and the neuroendocrine-immune axis: the pivotal role of glucocorticoids and lipocortin 1.British journal of pharmacology · 1996Review
- Induction of annexin-1 at transcriptional and post-transcriptional level in rat brain by methylprednisolone and the 21-aminosteroid U74389F.Mediators of inflammation · 1996Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The antiinflammatory actions of glucocorticoid steroids are thought to occur through induction of the protein lipocortin-1 (LC-1; annexin-1). The purpose of the current study was to investigate whether astrocytic LC-1 content was increased in the presence of a synthetic glucocorticoid, dexamethasone. 2. Steroid-induced changes in cellular levels of LC-1 in astrocytes were determined by electrotransfer and immunoblotting techniques. Separate cell fractions were investigated to study the influence of dexamethasone on astroglial LC-1 content. The effect of culture state on LC-1 expression was also examined. 3. Intracellular LC-1 content was found to decrease after initiation of culture, with a substantial rise in both cell proliferation and LC-1 expression occurring after the replenishment of medium containing steroid-free serum. A further increase in intracellular LC-1 occurred upon incubation with dexamethasone. The glucocorticoid-induced change in intracellular LC-1 was a time-dependent event and coincided with an increase in membrane-associated LC-1. 4. The findings in this study indicate that astrocytic LC-1 content is influenced by cell culture conditions and, in the presence of glucocorticoid steroids, the cellular localization of LC-1 is altered. This may indicate that LC-1 has functions at more than one cellular locality.
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