A new alternative NF-ΚB Pathway mediated the neuroprotection of GDNF on 6-OHDA-induced DA neurons neurotoxicity

Sun, Yu; Huang, Xu-Feng; Cao, Junping; Chen, Jing; Wang, Hongjun; Niu, Hongyan; Yu, Zhengquan; Yu, Jing-Kao; Wang, Ting; Hu, Yuan; Xu, Xiufen; Gao, Dianshuai

doi:10.1016/j.brainres.2011.12.021

Cited by 5 publications

(7 citation statements)

References 27 publications

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“…| 4115 up a conservative process against 6-OHDA-induce DA neuron apoptosis (Sun et al, 2012). Moreover, it is exhibited that transient GDNF expression, through NF-κB signaling, can trigger Pitx3 transcription, which is necessary for expression of brain-derived neurotrophic factor (BDNF) (Peng et al, 2011).…”

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confidence: 99%

Nuclear factor‐kappa B (NF‐κB) in pathophysiology of Parkinson disease: Diverse patterns and mechanisms contributing to neurodegeneration

Dolatshahi

Hameghavandi

Sabahi

et al. 2021

Eur J of Neuroscience

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Parkinson's disease (PD) is the second most common neurodegenerative disease and the most common movement disorder, which causes morbidity and mortality and imposes a large burden (Kowal et al., 2013). Sporadic form of PD occurs more abundantly in aging population and causes symptoms like rigidity, bradykinesia, akinesia, resting tremor, motor imbalance, etc (Davie, 2008). It is characterized by selective degeneration and progressive loss of dopaminergic (DA) neurons in substantia nigra pars compacta (SNpc) which give rise to axonal processes innervating striatum (Surmeier, 2018). A myriad of etiologies contribute to DA neuron loss including inflammation, oxidative stress, autophagy, neurotransmission alterations, metabolic changes, etc. However, the

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confidence: 99%

Nuclear factor‐kappa B (NF‐κB) in pathophysiology of Parkinson disease: Diverse patterns and mechanisms contributing to neurodegeneration

Dolatshahi

Hameghavandi

Sabahi

et al. 2021

Eur J of Neuroscience

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“…Notably, they observed reduced expression of GDNF. In other work, an inflammatory response upregulated GDNF expression (indeed, NF-κB mediated the neuroprotective effects of GDNF in other experimental models [5]), and the authors acknowledge that this may be the first work to demonstrate that neuroinflammation in this context reduces the release of GDNF. It is possible that anesthetics interfere with the inflammation-induced upregulation of GDNF that would otherwise be seen during surgical stress.…”

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confidence: 66%

Anesthetic neurotoxicity: an emerging role for glia in neuroprotection

Bell

Stary

2017

J Mol Med

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“…Additionally, constitutive NF-κB activity is required for the survival of neurons [ 146 ]. It has been proposed that the neuroprotective effects of glial cell line-derived neurotrophic factor (GDNF) on dopaminergic neurons is NF-κB-dependent [ 147 ]. These cells express NIK and GDNF induces IKKα-mediated phosphorylation of p100 and its subsequent processing to p52 [ 147 ].…”

Section: Relbmentioning

confidence: 99%

“…It has been proposed that the neuroprotective effects of glial cell line-derived neurotrophic factor (GDNF) on dopaminergic neurons is NF-κB-dependent [ 147 ]. These cells express NIK and GDNF induces IKKα-mediated phosphorylation of p100 and its subsequent processing to p52 [ 147 ]. Surprisingly, however, it was proposed that the p65/p52 heterodimers translocate to the nucleus and block apoptosis, and this process is independent of RelB [ 147 ].…”

Section: Relbmentioning

confidence: 99%

“…These cells express NIK and GDNF induces IKKα-mediated phosphorylation of p100 and its subsequent processing to p52 [ 147 ]. Surprisingly, however, it was proposed that the p65/p52 heterodimers translocate to the nucleus and block apoptosis, and this process is independent of RelB [ 147 ]. Of note, LTβ induces gliogenesis of neural progenitor cells/neural stem cells primarily through activation of the canonical NF-κB pathway and also induces RelB, but the implications of RelB activation remain unknown [ 148 ].…”

Section: Relbmentioning

confidence: 99%

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RelB and Neuroinflammation

Mockenhaupt

Gonsiewski

Kordula

2021

Cells

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Neuroinflammation within the central nervous system involves multiple cell types that coordinate their responses by secreting and responding to a plethora of inflammatory mediators. These factors activate multiple signaling cascades to orchestrate initial inflammatory response and subsequent resolution. Activation of NF-κB pathways in several cell types is critical during neuroinflammation. In contrast to the well-studied role of p65 NF-κB during neuroinflammation, the mechanisms of RelB activation in specific cell types and its roles during neuroinflammatory response are less understood. In this review, we summarize the mechanisms of RelB activation in specific cell types of the CNS and the specialized effects this transcription factor exerts during neuroinflammation.

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A new alternative NF-ΚB Pathway mediated the neuroprotection of GDNF on 6-OHDA-induced DA neurons neurotoxicity

Cited by 5 publications

References 27 publications

Nuclear factor‐kappa B (NF‐κB) in pathophysiology of Parkinson disease: Diverse patterns and mechanisms contributing to neurodegeneration

Nuclear factor‐kappa B (NF‐κB) in pathophysiology of Parkinson disease: Diverse patterns and mechanisms contributing to neurodegeneration

Anesthetic neurotoxicity: an emerging role for glia in neuroprotection

RelB and Neuroinflammation

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