Signalling pathway leading to an activation of mitogen-activated protein kinase by stimulating M3 muscarinic receptor

Kim, Jee Young; Yang, Myung-Soon; Oh, Chulhong; Kim, Kyong‐Tai; Ha, Mahn Joon; Kang, Shin‐Sung; Chun, Jang‐Soo

doi:10.1042/bj3370275

Cited by 44 publications

(23 citation statements)

References 35 publications

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“…Activation of the different MAPK pathways occurs simultaneously, and there is crosstalk between ERK1/2 and p38 that is mediated by various protein phosphatases [145,185]. Moreover, it has been demonstrated that PKC phosphorylates both ERK1/2 and p38 MAPK [76,86,153] providing a link between PKC and MAPK signaling. In the presence of functioning protein phosphatases, estrogens, via maintenance of protein phosphatase activity [200,201], or specific inhibitors of ERK1/2 or PKC [202] prevent glutamate death signaling.…”

Section: Mapk Pathway Involvement In Er-independent Estrogen-indumentioning

confidence: 99%

Role of protein phosphatases and mitochondria in the neuroprotective effects of estrogens

Simpkins

Yang

2009

Frontiers in Neuroendocrinology

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In the present treatise, we provide evidence that the neuroprotective and mito-protective effects of estrogens are inexorably linked and involve the ability of estrogens to maintain mitochondrial function during neurotoxic stress. This is achieved by the induction of nuclear and mitochondrial gene expression, the maintenance of protein phosphatases levels in a manner that likely involves modulation of the phosphorylation state of signaling kinases and mitochondrial pro- and anti-apoptotic proteins, and the potent redox/antioxidant activity of estrogens. These estrogen actions are mediated through a combination of estrogens receptor (ER)-mediated effects on nuclear and mitochondrial transcription of protein vital to mitochondrial function, ER-mediated, non-genomic signaling and non-ER-mediated effects of estrogens on signaling and oxidative stress. Collectively, these multifaceted, coordinated action of estrogens leads to their potency in protecting neurons from a wide variety of acute insults as well as chronic neurodegenerative processes.

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Section: Mapk Pathway Involvement In Er-independent Estrogen-indumentioning

confidence: 99%

Role of protein phosphatases and mitochondria in the neuroprotective effects of estrogens

Simpkins

Yang

2009

Frontiers in Neuroendocrinology

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“…To analyse the effects of endogenous Ras pathway activation on NADPH oxidase complex, we stimulated SK‐N‐BE cells with the cholinergic agonist carbachol. Under these conditions, the Ras/ERK1/2 pathway is activated through the stimulation of M3 muscarinic receptors that act on Ras via G q/11 /phospholipase C/protein kinase Cε pathway (Kim et al . 1999).…”

Section: Endogenous Ras Activation By Cholinergic Stimulation Of Sk‐nmentioning

confidence: 99%

HaRas activates the NADPH oxidase complex in human neuroblastoma cells via extracellular signal‐regulated kinase 1/2 pathway

Serù¹,

Mondola²,

Damiano³

et al. 2004

Journal of Neurochemistry

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In this study we have investigated the effects of the small GTP-binding-protein Ras on the redox signalling of the human neuroblastoma cell line, SK-N-BE stably transfected with HaRas(Val12). The levels of reactive oxygen species (ROS) and superoxide anions were significantly higher in HaRas(Val12) expressing (SK-HaRas) cells than in control cells. The treatment of cells with 4-(2-aminoethyl) benzenesulfonylfluoride, a specific inhibitor of the membrane superoxide generating system NADPH oxidase, suppressed the rise in ROS and significantly reduced superoxide levels produced by SK-HaRas cells. Moreover, HaRas(Val12) induced the translocation of the cytosolic components of the NADPH oxidase complex p67phox and Rac to the plasma membrane. These effects depended on the mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (MEK/ERK1/2) pathway, as the specific MEK inhibitor, PD98059, prevented HaRas-mediated increase in ROS and superoxide anions. In contrast, the specific phosphoinositide 3-kinase (PI3K) inhibitors LY294002 and wortmannin were unable to reverse the effects of HaRas(Val12). Moreover, cholinergic stimulation of neuroblastoma cells by carbachol, which activated endogenous Ras/ERK1/2, induced a significant increase in ROS levels and elicited membrane translocation of p67 phox and Rac. ROS generation induced by carbachol required the activation of ERK1/2 and PI3K. Hence, these data indicate that HaRas-induced ERK1/2 signalling selectively activates NADPH oxidase system in neuroblastoma cells.

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“…5B), indicating a lack of involvement of PKC α in this effect. In an additional experiment, astrocytoma cells were incubated with ingenol 3,20‐dibenzoate (IDB), a specific activator of PKC ϵ, which has been shown to downregulate this PKC isozyme selectively after prolonged incubation (Kim et al, 1999). A 24‐h preincubation with IDB caused a significant dose‐dependent reduction in carbachol‐mediated MAPK activation (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…There is also evidence that M 2 muscarinic receptors can stimulate MAPK, through the G βγ subunit (Crespo et al, 1994; Lopez‐Ilasaca et al, 1997). In case of M 2 receptors, the signaling to MAPK appears to involve Ras and phosphatidylinositol 3‐kinase (PI3K) (Crespo et al, 1994; Lopez‐Ilasaca et al, 1997), while for the other subtypes, an involvement of protein kinase C (PKC) has been suggested, albeit with contrasting results (Kim et al, 1999; Budd et al, 1999; Keely et al, 1998; Haring et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Evidence for two distinct mechanisms of neurogenesis and cellular pattern formation in regenerated goldfish retinas

et al. 2001

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After its destruction by intraocular injection of ouabain, the goldfish retina regenerates, but little is known about the histogenesis of the new tissue, including the structure and formation of regenerated cell mosaic patterns. In an effort to determine how retinal cells are generated and spatially organized within retina regenerated after ouabain injection, in situ hybridization and immunocytochemical techniques were combined with computational analyses of two-dimensional spatial patterns of identified neurons. Labeling with specific opsin riboprobes revealed two distinct cone patterns in the ouabain-injected eyes, each of which was different from the relatively orderly cone patterns of native retina. Central, regenerated regions had sparse aggregates of cones, and a relatively lower density of each cone type. Peripheral regions of experimental retina, likely derived from the circumferential germinal zone, had high densities of all cone types, each of which tended to be distributed randomly. The spatial patterns of inner retinal neurons in experimental eyes were also disorganized with respect to native retina. These results indicate that although some aspects of retinal regeneration resemble normal retinal development and growth, ouabain-induced regeneration does not produce well-organized mosaics of neurons, indicating a failure of the developmental interactions needed for proper pattern formation, which in turn could compromise visual recovery. Furthermore, the distinct cone patterns in different regions of experimental retina support the hypothesis that new goldfish retina arises via two spatially and cellularly distinct mechanisms after exposure to ouabain.

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Signalling pathway leading to an activation of mitogen-activated protein kinase by stimulating M3 muscarinic receptor

Cited by 44 publications

References 35 publications

Role of protein phosphatases and mitochondria in the neuroprotective effects of estrogens

Role of protein phosphatases and mitochondria in the neuroprotective effects of estrogens

HaRas activates the NADPH oxidase complex in human neuroblastoma cells via extracellular signal‐regulated kinase 1/2 pathway

Evidence for two distinct mechanisms of neurogenesis and cellular pattern formation in regenerated goldfish retinas

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