Emodin-induced microglial apoptosis is associated with TRB3 induction

Zhou, Xueping; Wang, Lili; Wang, Mingyan; Xu, Li; Yu, Li; Tai-hui, Fang; Mian-hua, WU

doi:10.3109/08923973.2010.549135

Cited by 27 publications

(26 citation statements)

References 32 publications

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“…Inhibition of apoptosis through mTOR also relies upon Akt activation. Cytoprotection through Akt can occur at several levels to foster cell survival through the maintenance of mitochondrial membrane potential, prevention of cytochrome c release and caspase activation, and regulate inflammatory cell activation (Hou et al , 2010a, b; Su et al , 2011; Zhang et al , 2012; Zhou et al , 2011). mTOR has been shown to require Akt activation to block apoptotic cell death (Hernandez et al , 2011; Magri et al , 2011; Shang et al , 2011, 2012) and require the inactivation of forkhead transcription factors, such as FoxO3a (Chong et al , 2011a; Dormond et al , 2007).…”

Section: Mtor and Cellular Demise With Oxidant Stress Apoptosis mentioning

confidence: 99%

Shedding new light on neurodegenerative diseases through the mammalian target of rapamycin

Chong¹,

Shang

Wang

et al. 2012

Progress in Neurobiology

105

118

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Neurodegenerative disorders affect a significant portion of the world's population leading to either disability or death for almost 30 million individuals worldwide. One novel therapeutic target that may offer promise for multiple disease entities that involve Alzheimer's disease, Parkinson's disease, epilepsy, trauma, stroke, and tumors of the nervous system is the mammalian target of rapamycin (mTOR). mTOR signaling is dependent upon the mTORC1 and mTORC2 complexes that are composed of mTOR and several regulatory proteins including the tuberous sclerosis complex (TSC1, hamartin/ TSC2, tuberin). Through a number of integrated cell signaling pathways that involve those of mTORC1 and mTORC2 as well as more novel signaling tied to cytokines, Wnt, and forkhead, mTOR can foster stem cellular proliferation, tissue repair and longevity, and synaptic growth by modulating mechanisms that foster both apoptosis and autophagy. Yet, mTOR through its proliferative capacity may sometimes be detrimental to central nervous system recovery and even promote tumorigenesis. Further knowledge of mTOR and the critical pathways governed by this serine/threonine protein kinase can bring new light for neurodegeneration and other related diseases that currently require new and robust treatments.

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Section: Mtor and Cellular Demise With Oxidant Stress Apoptosis mentioning

confidence: 99%

Shedding new light on neurodegenerative diseases through the mammalian target of rapamycin

Chong¹,

Shang

Wang

et al. 2012

Progress in Neurobiology

105

118

View full text Add to dashboard Cite

show abstract

“…PI 3-K and Akt can promote cellular proliferation and block apoptotic injury either alone or through pathways that involve EPO. In regards to the nervous system, activation of PI 3-K and Akt can promote endothelial survival [66,68,69,72,100,101,195,196], prevent cell injury in inflammatory cells [77,105,165,197–200], and block neuronal injury [58,157,179,201–205]. Akt also can limit apoptosis through the phosphorylation of FoxO proteins [206–210].…”

Section: Epo and Novel Neuroprotective Pathwaysmentioning

confidence: 99%

Erythropoietin: New Directions for the Nervous System

Maiese

Chong

Shang

et al. 2012

IJMS

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New treatment strategies with erythropoietin (EPO) offer exciting opportunities to prevent the onset and progression of neurodegenerative disorders that currently lack effective therapy and can progress to devastating disability in patients. EPO and its receptor are present in multiple systems of the body and can impact disease progression in the nervous, vascular, and immune systems that ultimately affect disorders such as Alzheimer’s disease, Parkinson’s disease, retinal injury, stroke, and demyelinating disease. EPO relies upon wingless signaling with Wnt1 and an intimate relationship with the pathways of phosphoinositide 3-kinase (PI 3-K), protein kinase B (Akt), and mammalian target of rapamycin (mTOR). Modulation of these pathways by EPO can govern the apoptotic cascade to control β-catenin, glycogen synthase kinase-3β, mitochondrial permeability, cytochrome c release, and caspase activation. Yet, EPO and each of these downstream pathways require precise biological modulation to avert complications associated with the vascular system, tumorigenesis, and progression of nervous system disorders. Further understanding of the intimate and complex relationship of EPO and the signaling pathways of Wnt, PI 3-K, Akt, and mTOR are critical for the effective clinical translation of these cell pathways into robust treatments for neurodegenerative disorders.

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“…PI 3-K and especially Akt1 are central to the regulation of cell growth and survival throughout the body [14, 30, 34, 43, 62–71]. WISP1 in non-neuronal systems has been shown to rely upon the PI 3-K and Akt signaling [22–25].…”

Section: Discussionmentioning

confidence: 99%

“…In addition, given the dependence of WISP1 on the PI 3-K and Akt1 pathways, it is known that the cytoprotective pathways promoted by PI 3-K and Akt1 have been tied to the modulation of mitochondrial permeability and cytochrome c release [14, 30, 66, 69, 71]. We therefore examined the ability of WISP1 to modulate mitochondrial membrane permeability and related apoptotic pathways.…”

Section: Discussionmentioning

confidence: 99%

Wnt1 Inducible Signaling Pathway Protein 1 (WISP1) Blocks Neurodegeneration through Phosphoinositide 3 Kinase/Akt1 and Apoptotic Mitochondrial Signaling Involving Bad, Bax, Bim, and Bcl-xL

Wang¹,

Chong²,

Shang³

et al. 2012

CNR

109

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Wnt1 inducible signaling pathway protein 1 (WISP1) is a member of the CCN family of proteins that determine cell growth, cell differentiation, immune system activation, and cell survival in tissues ranging from the cardiovascular-pulmonary system to the reproductive system. Yet, little is known of the role of WISP1 as a neuroprotective entity in the nervous system. Here we demonstrate that WISP1 is present in primary hippocampal neurons during oxidant stress with oxygen-glucose deprivation (OGD). WISP1 expression is significantly enhanced during OGD exposure by the cysteine-rich glycosylated protein Wnt1. Similar to the neuroprotective capabilities known for Wnt1 and its signaling pathways, WISP1 averts neuronal cell injury and apoptotic degeneration during oxidative stress exposure. WISP1 requires activation of phosphoinositide 3-kinase (PI 3-K) and Akt1 pathways to promote neuronal cell survival, since blockade of these pathways abrogates cellular protection. Furthermore, WISP1 through PI 3-K and Akt1 phosphorylates Bad and GSK-3β, minimizes expression of the Bim/Bax complex while increasing the expression of Bcl-xL/Bax complex, and prevents mitochondrial membrane permeability, cytochrome c release, and caspase 3 activation in the presence of oxidant stress. These studies provide novel considerations for the development of WISP1 as an effective and robust therapeutic target not only for neurodegenerative disorders, but also for disease entities throughout the body.

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Emodin-induced microglial apoptosis is associated with TRB3 induction

Cited by 27 publications

References 32 publications

Shedding new light on neurodegenerative diseases through the mammalian target of rapamycin

Shedding new light on neurodegenerative diseases through the mammalian target of rapamycin

Erythropoietin: New Directions for the Nervous System

Wnt1 Inducible Signaling Pathway Protein 1 (WISP1) Blocks Neurodegeneration through Phosphoinositide 3 Kinase/Akt1 and Apoptotic Mitochondrial Signaling Involving Bad, Bax, Bim, and Bcl-xL

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