Prevention of endoplasmic reticulum stress-induced cell death by brain-derived neurotrophic factor in cultured cerebral cortical neurons

Shimoke, Koji; Utsumi, Takahiro; Kishi, Soichiro; Nishimura, Manabu; Sasaya, Harue; Kudo, Motoshige; Ikeuchi, Toshihiko

doi:10.1016/j.brainres.2004.09.005

Cited by 48 publications

(31 citation statements)

References 28 publications

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“…In vitro and in vivo studies indicate that BDNF functions as a neuroprotective agent and rescues neurons from various insults [55,56] . Increasing evidence has shown that BDNF plays an important role in counteracting ER stress [35][36][37] , suggesting that the suppression of ER stress may contribute to BDNF-mediated neuroprotection. The action of BDNF is mediated by its binding to the TrkB receptor.…”

Section: Discussionmentioning

confidence: 99%

“…Brain-derived neurotrophic factor (BDNF), a neurotrophic factor acting on the central nervous system, prevents ordinary types of neuronal cell death induced by various stimulants. Increasing evidence has demonstrated that prevention of ER stress contributes to BDNF-mediated neuroprotection [35][36][37] . Therefore, the present study was undertaken to examine whether H 2 S could regulate Hcy-induced neuronal ER stress in a rat model of Hcy neurotoxicity in vivo.…”

Section: Introductionmentioning

confidence: 99%

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Hydrogen sulfide inhibits homocysteine-induced endoplasmic reticulum stress and neuronal apoptosis in rat hippocampus via upregulation of the BDNF-TrkB pathway

Wei

et al. 2014

Acta Pharmacol Sin

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Aim: Homocysteine (Hcy) can elicit neuronal cell death, and hyperhomocysteinemia is a strong independent risk factor for Alzheimer's disease. The aim of this study was to examine the effects of hydrogen sulfide (H 2 S) on Hcy-induced endoplasmic reticulum (ER) stress and neuronal apoptosis in rat hippocampus. Methods: Adult male SD rats were intracerebroventricularly (icv) injected with Hcy (0.6 μmol/d) for 7 d. Before Hcy injection, the rats were treated with NaHS (30 or 100 μmol·kg -1 ·d -1 , ip) and/or k252a (1 μg/d, icv) for 2 d. The apoptotic neurons were detected in hippocampal coronal slices with TUNEL staining. The expression of glucose regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), cleaved caspase-12, and BDNF in the hippocampus were examined using Western blotting assays. The generation of H 2 S in the hippocampus was measured with the NNDPD method. Results: Hcy markedly inhibited the production of endogenous H 2 S and increased apoptotic neurons in the hippocampus. Furthermore, Hcy induced ER stress responses in the hippocampus, as indicated by the upregulation of GRP78, CHOP, and cleaved caspase-12. Treatment with the H 2 S donor NaHS increased the endogenous H 2 S production and BDNF expression in a dosedependent manner, and significantly reduced Hcy-induced neuronal apoptosis and ER stress responses in the hippocampus. Treatment with k252a, a specific inhibitor of TrkB (the receptor of BDNF), abolished the protective effects of NaHS against Hcy-induced ER stress in the hippocampus. Conclusion: H 2 S attenuates ER stress and neuronal apoptosis in the hippocampus of Hcy-treated rats via upregulating the BDNF-TrkB pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Hydrogen sulfide inhibits homocysteine-induced endoplasmic reticulum stress and neuronal apoptosis in rat hippocampus via upregulation of the BDNF-TrkB pathway

Wei

et al. 2014

Acta Pharmacol Sin

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“…Apart from these proteins, ER stress and caspase-12 activation in neurons is influenced by the presence of the neuronal calcium-binding protein, hippocalcin and by upstream signals elicited by brain-derived neurotrophic factor. 27,28 There are probably other proteins and interactions yet to be discovered that take part in the ER-mitochondria crosstalk and in the control of cell death by the ER.…”

Section: Introductionmentioning

confidence: 99%

ER stress and neurodegenerative diseases

2006

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“…MAP kinase signaling also clearly contributed to neurite outgrowth in PC12 cells, based on the effects of PD and U, indicating that at least two signaling pathways are involved in neurite elongation. These pathways also promote cell survival because cells treated with fsk remained fresh and alive (Figure-1A) [15,16]. Both may contribute to rescue from cell death because Tm is well known to induce ER stress-mediated cell death by accumulation of unfolded proteins.…”

Section: Resultsmentioning

confidence: 99%

Genomic Control of Upregulation of GRP78 Expression for Promotion of Neurite Elongation and Attenuation of Cell Death via PKA-Mediated Signaling in PC12 Cells

Yamazoe¹,

Nishihata²,

Nakagawa³

2015

Clin Pharmacol Biopharm

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Neurodegeneration occurs due to neuronal cell death and subsequently disrupts neuronal networks. In current medicine, methods for interruption of neuronal cell death and avoidance of disruption of neuronal networks have potential as therapy for neurodegenerative disorders. Development of this therapy requires analysis of the molecular mechanism of neurite extension that leads to network formation. Here, we show that forskolin (fsk), an activator of adenylate cyclase, increases the intracellular cAMP concentration and induces neurite outgrowth in PC12 cells. The effect of fsk on neurite outgrowth was diminished by H89, an inhibitor of protein kinase A (PKA), and by PD98059 and U0126, which are inhibitors of the mitogen-activated protein kinase (MAPK) signaling pathway. With fsk treatment in the presence of tunicamycin, an inducer of cell death, the activity of the glucose-regulated protein 78 (GRP78) promoters was upregulated. Interestingly, this effect was completely abolished by H89 and by PD98059 and U0126. This phenomenon was confirmed using a dominant-negative PKA-expressing PC12 cell line, in which the PKA-mediated signaling pathway was completely eliminated. These lines of evidence suggest that GRP78 promotes neuronal elongation that is regulated by fsk and mediated by PKA.

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Prevention of endoplasmic reticulum stress-induced cell death by brain-derived neurotrophic factor in cultured cerebral cortical neurons

Cited by 48 publications

References 28 publications

Hydrogen sulfide inhibits homocysteine-induced endoplasmic reticulum stress and neuronal apoptosis in rat hippocampus via upregulation of the BDNF-TrkB pathway

Hydrogen sulfide inhibits homocysteine-induced endoplasmic reticulum stress and neuronal apoptosis in rat hippocampus via upregulation of the BDNF-TrkB pathway

ER stress and neurodegenerative diseases

Genomic Control of Upregulation of GRP78 Expression for Promotion of Neurite Elongation and Attenuation of Cell Death via PKA-Mediated Signaling in PC12 Cells

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