Differential expression of sgk mRNA, a member of the Ser/Thr protein kinase gene family, in rat brain after CNS injury

Imaizumi, Kazunori; Tsuda, Manabu; Wanaka, Akio; Tohyama, Masaya; Takagi, Tsutomu

doi:10.1016/0169-328x(94)90090-6

Cited by 113 publications

(73 citation statements)

References 26 publications

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“…Moreover, the physiological stress hormones, glucocorticoids, stimulate sgk promoter activity through a glucocorticoid response element, and sgk is a transcriptional target of the p53 tumor suppressor gene, a known target of genotoxic stress (28,32). Consistent with a role for Sgk in the cellular stress response, sgk transcripts have been shown to be elevated in response to ischemic injury of the brain, changes in cell volume, and inflammatory disease and in a screen for transcripts involved in wound repair in fibroblasts (33)(34)(35)(36). Therefore, to determine whether transcription of the sgk gene is a component of the stress response in mammalian cells, the hyperosmolar regulation of Sgk was examined in mammary epithelial cells.…”

mentioning

confidence: 75%

Hyperosmotic Stress Stimulates Promoter Activity and Regulates Cellular Utilization of the Serum- and Glucocorticoid-inducible Protein Kinase (Sgk) by a p38 MAPK-dependent Pathway

Bell¹,

Leong²,

Kim³

et al. 2000

Journal of Biological Chemistry

143

149

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We have established that the serum-and glucocorticoid-inducible protein kinase (Sgk) is a new component of the hyperosmotic stress response. Treatment of NMuMg mammary epithelial cells with the organic osmolyte, sorbitol, caused the stable accumulation of Sgk transcripts and protein after an approximately 4-h lag. Transient transfection of a series of sgk-CAT reporter plasmids containing either 5 deletions or continuous 6-base pair substitutions identified a hyperosmotic stress-regulated element that is GC-rich and is necessary for the sorbitol stimulation of sgk gene promoter activity. Gel shift analysis identified four major DNAprotein complexes in the hyperosmotic stress-regulated element that, by competition with excess consensus wild type and mutant oligonucleotides and by antibody supershifts, contains the Sp1 transcription factor. Several lines of evidence suggest that the p38 MAPK signaling pathway mediates the hyperosmotic stress stimulation of sgk gene expression. Treatment with pharmacological inhibitors of p38 MAPK or with a dominant negative form of MKK3, an upstream regulator of p38 MAPK, significantly reduced or ablated the sorbitol induction of sgk promoter activity or protein production. Using an in vitro peptide transphosphorylation assay, sorbitol treatment activates either endogenous or exogenous Sgk that is localized to the cytoplasmic compartment. Thus, we propose that the stimulated expression of enzymatically active Sgk after sorbitol treatment is a newly defined component of the p38 MAPK-mediated response to hyperosmotic stress.

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mentioning

confidence: 75%

Hyperosmotic Stress Stimulates Promoter Activity and Regulates Cellular Utilization of the Serum- and Glucocorticoid-inducible Protein Kinase (Sgk) by a p38 MAPK-dependent Pathway

Bell¹,

Leong²,

Kim³

et al. 2000

Journal of Biological Chemistry

143

149

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“…SGK, a serine/threonine protein kinase with sequence similarity to AKT (also called protein kinase B), was identified originally on the basis of its transcriptional upregulation in vitro in response to glucocorticoids and serum (Webster et al, 1993a). In vitro studies indicate that, in addition to serum and/or glucocorticoids, the transcription of SGK also is influenced by hormones such as follicle-stimulating hormone (FSH) (Alliston et al, 2000) and aldosterone (Chen et al, 1999), injury (Imaizumi et al, 1994), cell volume changes (Waldegger et al, 1997;Bell et al, 2000), and heparin (Delmolino and Castellot, 1997). One possibility is that stress accompanying launching, prolonged existence in microgravity, and/or landing could produce elevated glucocorticoid levels (Macho et al, 1993;Stein et al, 1999) and thereby induce SGK expression.…”

Section: Discussionmentioning

confidence: 99%

Expression of Serum- and Glucocorticoid-Inducible Kinase Is Regulated in an Experience-Dependent Manner and Can Cause Dendrite Growth

David¹,

Stegenga²,

Hu³

et al. 2005

J. Neurosci.

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The interaction of an animal with its environment during a critical period in early postnatal life has lifelong effects on the structure and function of sensory and motor systems. To gain insight into the molecular mechanisms of experience-dependent development, we challenged young rats to adapt to a new environment that engenders novel motor behavior. Rats born in the gravitational field (1G) of the earth subsequently were reared for 2 weeks either in the absence of gravity (microgravity) or at 1G. A comparison of gene expression using microarrays led to the identification of a panel of differentially regulated transcripts. We report here that the abundance of serum-and glucocorticoid-inducible kinase (SGK) is increased in spinal cord tissue from animals reared in microgravity in comparison with 1G-reared controls. The induction of SGK expression also can be achieved by administration of glucocorticoids to animals at 1G or neurons in vitro. Expression of constitutively active SGK in neurons leads to the elaboration of neuronal dendrites and their branching. Glucocorticoids also lead to dendrite elaboration, and this effect can be abrogated by inhibiting SGK activity. Changes in the level of expression of SGK could be part of the mechanism for experience-dependent acquisition of mature neuronal properties.

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“…91,92 Sgk1 is similar in primary structure to protein kinase B (PKB), protein kinase C (PKC) and protein kinase A (PKA). In the brain or in brain cells, transcription of Sgk1 is increased in several animal models of Parkinson's disease 93 and a transgenic model of amyotrophic lateral sclerosis (ALS), following brain injury 94 and after transient global cerebral ischemia. 95 Increased expression of Sgk1 has been observed in the Hippo of fast-learning rats as compared with slow-learning rats.…”

Section: Number Of Transcripts Affected By Single and Multiple Treatmmentioning

confidence: 99%

Region-specific transcriptional changes following the three antidepressant treatments electro convulsive therapy, sleep deprivation and fluoxetine

et al. 2006

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The significant proportion of depressed patients that are resistant to monoaminergic drug therapy and the slow onset of therapeutic effects of the selective serotonin reuptake inhibitors (SSRIs)/serotonin/noradrenaline reuptake inhibitors (SNRIs) are two major reasons for the sustained search for new antidepressants. In an attempt to identify common underlying mechanisms for fast-and slow-acting antidepressant modalities, we have examined the transcriptional changes in seven different brain regions of the rat brain induced by three clinically effective antidepressant treatments: electro convulsive therapy (ECT), sleep deprivation (SD), and fluoxetine (FLX), the most commonly used slow-onset antidepressant. Each of these antidepressant treatments was applied with the same regimen known to have clinical efficacy: 2 days of ECT (four sessions per day), 24 h of SD, and 14 days of daily treatment of FLX, respectively. Transcriptional changes were evaluated on RNA extracted from seven different brain regions using the Affymetrix rat genome microarray 230 2.0. The gene chip data were validated using in situ hybridization or autoradiography for selected genes. The major findings of the study are:1. The transcriptional changes induced by SD, ECT and SSRI display a regionally specific distribution distinct to each treatment. 2. The fast-onset, short-lived antidepressant treatments ECT and SD evoked transcriptional changes primarily in the catecholaminergic system, whereas the slow-onset antidepressant FLX treatment evoked transcriptional changes in the serotonergic system. 3. ECT and SD affect in a similar manner the same brain regions, primarily the locus coeruleus, whereas the effects of FLX were primarily in the dorsal raphe and hypothalamus, suggesting that both different regions and pathways account for fast onset but short lasting effects as compared to slow-onset but long-lasting effects. However, the similarity between effects of ECT and SD is somewhat confounded by the fact that the two treatments appear to regulate a number of transcripts in an opposite manner. 4. Multiple transcripts (e.g. brain-derived neurotrophic factor (BDNF), serum/glucocorticoidregulated kinase (Sgk1)), whose level was reported to be affected by antidepressants or behavioral manipulations, were also found to be regulated by the treatments used in the present study. Several novel findings of transcriptional regulation upon one, two or all three treatments were made, for the latter we highlight homer, erg2, HSP27, the proto oncogene ret, sulfotransferase family 1A (Sult1a1), glycerol 3-phosphate dehydrogenase (GPD3), the orphan receptor G protein-coupled receptor 88 (GPR88) and a large number of expressed sequence tags (ESTs). 5. Transcripts encoding proteins involved in synaptic plasticity in the hippocampus were strongly affected by ECT and SD, but not by FLX.The novel transcripts, concomitantly regulated by several antidepressant treatments, may represent novel targets for fast onset, long-duration antidepressants.

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Differential expression of sgk mRNA, a member of the Ser/Thr protein kinase gene family, in rat brain after CNS injury

Cited by 113 publications

References 26 publications

Hyperosmotic Stress Stimulates Promoter Activity and Regulates Cellular Utilization of the Serum- and Glucocorticoid-inducible Protein Kinase (Sgk) by a p38 MAPK-dependent Pathway

Hyperosmotic Stress Stimulates Promoter Activity and Regulates Cellular Utilization of the Serum- and Glucocorticoid-inducible Protein Kinase (Sgk) by a p38 MAPK-dependent Pathway

Expression of Serum- and Glucocorticoid-Inducible Kinase Is Regulated in an Experience-Dependent Manner and Can Cause Dendrite Growth

Region-specific transcriptional changes following the three antidepressant treatments electro convulsive therapy, sleep deprivation and fluoxetine

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