Alteration of serum/glucocorticoid regulated kinase-1 (sgk-1) gene expression in rat hippocampus after transient global ischemia

Nishida, Yusuke; Nagata, Toshihito; Takahashi, Yasuo; Sugahara-Kobayashi, Megumi; Murata, Akiko; Asai, Satoshi

doi:10.1016/j.molbrainres.2004.01.008

Cited by 57 publications

(47 citation statements)

References 11 publications

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“…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. 96 Enrichment-induced Sgk1 expression is specifically mediated through alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors 97 and Sgk1 can directly phosphorylate the transcription factor cyclic AMP response element-binding protein (CREB) on serine 133.…”

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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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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“…Notably, SGK1 expression is upregulated by cerebral ischemia (46) and may help to enhance cellular glucose uptake into the ischemic tissue. Moreover, the enhanced cerebral SGK1 expression in enriched environment (47) may serve to adjust glucose uptake to the enhanced demand following stimulation of neuronal activity.…”

Section: Fig 8 Glucose Transport Is Reduced In Adipocytes Isolated mentioning

confidence: 99%

SGK1 Kinase Upregulates GLUT1 Activity and Plasma Membrane Expression

et al. 2006

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Phosphatidylinositol 3-kinase (PI3 kinase) inhibition disrupts the ability of insulin to stimulate GLUT1 and GLUT4 translocation into the cell membrane and thus glucose transport. The effect on GLUT4 but not on GLUT1 is mediated by activation of protein kinase B (PKB). The serum-and glucocorticoid-inducible kinase SGK1, a further kinase downstream of PI3 kinase, regulates several transporters by enhancing their plasma membrane abundance. GLUT1 contains a consensus site ( 95 Ser) for phosphorylation by SGK1. Thus, the present study investigated whether GLUT1 is regulated by the kinase. Tracer-flux studies in Xenopus oocytes and HEK-293 cells demonstrated that GLUT1 transport is enhanced by constitutively active S422D SGK1. The effect requires the kinase catalytical activity since the inactive mutant K127N SGK1 failed to modulate GLUT1. GLUT1 stimulation by S422D SGK1 is not due to de novo protein synthesis but rather to an increase of the transporter's abundance in the plasma membrane. Kinetic analysis revealed that SGK1 enhances maximal transport rate without altering GLUT1 substrate affinity. These observations suggest that SGK1 regulates GLUT1 and may contribute to or account for the PI3 kinasedependent but PKB-independent stimulation of GLUT1 by insulin. Diabetes 55:421-427, 2006 I nsulin stimulates glucose transport in hormoneresponsive tissues mainly by inducing the redistribution of the facilitated hexose carrier isoforms GLUT1 (SLC2A1) and GLUT4 (SLC2A4) from intracellular compartments to the plasma membrane (1-3). The cascade of signaling events involved in glucose transporter trafficking to the cell surface in response to insulin is triggered by an increase in insulin receptor tyrosine kinase activity followed by tyrosine phosphorylation of insulin receptor substrate proteins and activation of phosphatidylinositol 3-kinase (PI3 kinase). Downstream elements of PI3 kinase include the phosphoinositide-dependent kinase PDK1, which in turn phosphorylates and thus activates the serine/threonine kinase Akt/protein kinase B (PKB) (4 -6).The role of PI3 kinase in insulin-dependent and -independent stimulation of GLUT1 and GLUT4 translocation has been confirmed by several studies using pharmacological (Wortmannin and LY294002) blockade and genetic (PI3 kinase dominant-negative mutants) knockout of the kinase (7-11). The effect of PI3 kinase on GLUT4 trafficking is mediated by PKB (12,13). PKB is, however, at least in some cells, not required for the PI3 kinase-dependent trafficking of GLUT1 (12). Thus, some other PI3 kinasedependent protein kinases are presumably involved in the regulation of GLUT1.A further downstream molecule in the PI3 kinase signaling cascade is the serum-and glucocorticoid-inducible kinase SGK1. SGK1 was originally cloned as a glucocorticoid-sensitive gene from rat mammary tumor cells (14) and later as a human cell volume-regulated gene (15). SGK1 shares ϳ80% homology with its isoforms SGK2 and SGK3 (16) and ϳ60% homology with PKB (17).To become catalytically active, SGK1 requires phosphoryl...

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“…High levels of SGK1 mRNA have been observed in ischemia (7), injury (8), in various animal models of Parkinson's disease (9,10), amyotrophic lateral sclerosis (11), Rett syndrome (12,13), Huntington's disease (14), and in the dorsal horn of the spinal cord after induction of inflammation in the corresponding innervated peripheral tissues (15).…”

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confidence: 99%

A brain-specific SGK1 splice isoform regulates expression of ASIC1 in neurons

Arteaga

Ćorić

Straub

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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Neurodegenerative diseases and noxious stimuli to the brain enhance transcription of serum-and glucocorticoid-induced kinase-1 (SGK1). Here, we report that the SGK1 gene encodes a brain-specific additional isoform, SGK1.1, which exhibits distinct regulation, properties, and functional effects. SGK1.1 decreases expression of the acid-sensing ion channel-1 (ASIC1); thereby, SGK1.1 may limit neuronal injury associated to activation of ASIC1 in ischemia. Given that neurons express at least two splice isoforms, SGK1 and SGK1.1, driven by distinct promoters, any changes in SGK1 transcript level must be examined to define the isoform induced by each stimulus or neurological disorder.alternative promoter ͉ Proton-activated channel ͉ serum-and glucocorticoid-induced kinase

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Alteration of serum/glucocorticoid regulated kinase-1 (sgk-1) gene expression in rat hippocampus after transient global ischemia

Cited by 57 publications

References 11 publications

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

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

SGK1 Kinase Upregulates GLUT1 Activity and Plasma Membrane Expression

A brain-specific SGK1 splice isoform regulates expression of ASIC1 in neurons

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