Serum‐ and glucocorticoid‐inducible kinase (SGK) is a target of the MAPK/ERK signaling pathway that mediates memory formation in rats

Lee, Ching-Tien; Tyan, Shiaw-Wei; Ma, Yun‐Li; Tsai, Ming-Chi; Yang, Ying; Lee, Eminy H.Y.

doi:10.1111/j.1460-9568.2006.04650.x

Cited by 33 publications

(29 citation statements)

References 38 publications

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“…22,23 Mechanical stretch stimulated strong phosphorylation of extracellular signal-regulated kinase (ERK)1/2 and p38, and moderate phosphorylation of c-Jun N-terminal kinase (JNK) ( Figure 2A). We then inhibited different MAPKs in venous SMC and found that inhibition of MEK1 with inhibitor (U0126) or MEK1 dominant negative, but not inhibitor of p38 or JNK, significantly inhibited stretch-induced increases in SGK-1 protein level (Figure 2B and 2C).…”

Section: Mek1 Signaling Pathway Mediates Mechanical Stretch-induced Smentioning

confidence: 99%

The Mechanical Stress–Activated Serum-, Glucocorticoid-Regulated Kinase 1 Contributes to Neointima Formation in Vein Grafts

Cheng

Wang

et al. 2010

Circulation Research

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Objective: The objective of this study is to identify mechanisms of mechanical stretch on neointima formation. Methods and Results: By a microarray analysis, we found that mechanical cyclic stretch (15% elongation) stimulated the transcription of SGK-1 (serum-, glucocorticoid-regulated kinase-1). Mechanical stretch-induced SGK-1 mRNA expression was blocked by actinomycin D. The mechanism for the SGK-1 expression involved MEK1 but not p38 or JNK signaling pathway. SGK-1 activation in response to stretch is blocked by insulin-like growth factor (IGF)-1 receptor inhibitor and mammalian target of rapamycin complex (mTORC)2 inhibitor (Ku-0063794) but not mTORC1 inhibitor (rapamycin). Mechanical stretch-induced bromodeoxyuridine incorporation was reduced by 83.5% in venous SMCs isolated from SGK-1 knockout mice. In contrast, inhibition of Akt, another downstream signal of PI3K resulted in only partial inhibition of mechanical stretch-induced proliferation of venous SMCs. Mechanical stretch also induced phosphorylation and nuclear exportation of p27 kip1 , whereas knockout of SGK-1 attenuated this effect of mechanical stretch on p27 kip1. In vivo, we found that placement of a vein graft into artery increased SGK-1 expression. Knockout of SGK-1 effectively prevented neointima formation in vein graft. There is significant lower level of p27 kip1 located in the nucleus of neointima cells in SGK-1 knockout mice compared with that of wild-type vein graft. In addition, we also found that wire injury of artery or growth factors in vitro increased expression of SGK-1. Key Words: mechanical stretch Ⅲ serum-, glucocorticoid-regulated kinase-1 Ⅲ neointima formation Ⅲ mTORC Ⅲ mammalian target of rapamycin complex I ncreased growth of venous smooth muscle cells (SMCs) is a hallmark of vein graft failure. [1][2][3][4] After implantation of a vein graft into the arterial circulation, the venous wall is immediately exposed to mechanical stimuli. Those include arterial pressure, wall tension, shear stress, and pulsatile flow, all of which modulate graft physiology. [5][6][7] Such alteration could lead to the activation of many intracellular signaling pathways. Mechanical stress could also stimulate the synthesis and/or secretion of various bioactive molecules including platelet-derived growth factor (PDGF), basic fibroblast growth factor, and the transcriptional factors. 8 -10 Recently, we have shown that mechanical stretch stimulates expression and activation of insulin-like growth factor (IGF)-1 and its receptor in venous SMCs, and we found that activated IGF-1R/phosphatidylinositol 3-kinase (PI3K) is essential for mechanical stretch-induced proliferation of venous SMCs. 11 However, the downstream targets of IGF-1/ PI3K signaling that mediate mechanical stretch-induced proliferation of venous SMCs are still unknown. Conclusions:Belonging to the AGC subfamily, the catalytic domain of SGK-1 (serum-, glucocorticoid-regulated kinase-1) is 54% identical to that of AKT, and it shares common downstream substrates with AKT. 12,13 Activation...

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Section: Mek1 Signaling Pathway Mediates Mechanical Stretch-induced Smentioning

confidence: 99%

The Mechanical Stress–Activated Serum-, Glucocorticoid-Regulated Kinase 1 Contributes to Neointima Formation in Vein Grafts

Cheng

Wang

et al. 2010

Circulation Research

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“…Serum-and glucocorticoidinducible kinase (SGK) is another downstream target of PI-3K-PDK1 (phosphoinositide-dependent protein kinase-1) signaling (Kobayashi and Cohen, 1999). SGK1 has recently been demonstrated to play an important role in spatial memory formation (Tsai et al, 2002;Lee et al, 2006). A higher SGK mRNA level was found in fast-learning rats than slow-learning rats in the water maze learning task.…”

Section: Introductionmentioning

confidence: 96%

“…Plasmid DNA was constructed as described previously (Chao et al, 2006;Lee et al, 2006). The sgk gene has different isoforms, and here we examined sgk1.…”

Section: Methodsmentioning

confidence: 99%

Protein Kinase CK2 Impairs Spatial Memory Formation through Differential Cross Talk with PI-3 Kinase Signaling: Activation of Akt and Inactivation of SGK1

Chao¹,

Ma²,

Lee³

2007

Journal of Neuroscience

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Casein kinase II (CK2) is a multifunctional serine/threonine protein kinase that is associated with the development of neuritogenesis and synaptic plasticity. The phosphoinositide 3-kinase (PI-3K)/Akt pathway is implicated in long-term memory formation. In addition, serum-and glucocorticoid-inducible kinase 1 (SGK1) is another downstream target of PI-3K signaling that was shown to play an important role in spatial memory formation. Whether CK2 may also affect memory formation and whether CK2 interacts with Akt and SGK1 during this process is unknown. In the present study, we found that water maze training significantly decreased CK2 activity in the rat hippocampal CA1 area but not in the dentate gyrus (DG) area. Transfection of the dominant negative mutant of CK2, CK2␣A 156 , to the CA1 area, but not to the DG area, decreased CK2 activity but enhanced spatial memory formation. Meanwhile, it increased SGK1 phosphorylation at Ser422, decreased Akt phosphorylation at Ser473, and increased cAMP response element-binding protein phosphorylation at Ser133. Transfection of the constitutively active SGK1, SGKS422D, enhanced whereas transfection of the wild-type Akt impaired spatial memory formation. Also, administration of the protein phosphatase 2A inhibitor, fostriecin, reversed the memory-impairing effect of CK2␣WT. It also reversed the effect of CK2␣WT in decreasing SGK1 phosphorylation. Akt Ser473 phosphorylation was moderately increased by CK2␣WT and fostriecin treatment, but AktS473A mutant transfection reversed the memory-impairing effect of CK2␣WT. These results together suggest that CK2 impairs spatial memory formation through differential cross talk with PI-3 kinase signaling by activation of Akt and inactivation of SGK1 through protein phosphatase 2A.

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“…PDK1 phosphorylates SGK1 at threonine-256, which is required in hippocampal area CA1 for spatial memory formation (Lee et al 2006). Further, SGK1 is phosphorylated at serine-78 by ERK (Lee et al 2006). This phosphorylation is not important for spatial memory formation but it is required for contextual fear LTM formation ).…”

Section: Pi3kmentioning

confidence: 99%

The roles of protein kinases in learning and memory

2013

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In the adult mammalian brain, more than 250 protein kinases are expressed, but only a few of these kinases are currently known to enable learning and memory. Based on this information it appears that learning and memory-related kinases either impact on synaptic transmission by altering ion channel properties or ion channel density, or regulate gene expression and protein synthesis causing structural changes at existing synapses as well as synaptogenesis. Here, we review the roles of these kinases in short-term memory formation, memory consolidation, memory storage, retrieval, reconsolidation, and extinction. Specifically, we discuss the roles of calcium/calmodulin-dependent kinase II (CaMKII

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Serum‐ and glucocorticoid‐inducible kinase (SGK) is a target of the MAPK/ERK signaling pathway that mediates memory formation in rats

Cited by 33 publications

References 38 publications

The Mechanical Stress–Activated Serum-, Glucocorticoid-Regulated Kinase 1 Contributes to Neointima Formation in Vein Grafts

The Mechanical Stress–Activated Serum-, Glucocorticoid-Regulated Kinase 1 Contributes to Neointima Formation in Vein Grafts

Protein Kinase CK2 Impairs Spatial Memory Formation through Differential Cross Talk with PI-3 Kinase Signaling: Activation of Akt and Inactivation of SGK1

The roles of protein kinases in learning and memory

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