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Cited by 80

Regulatory effects of neuroinflammatory responses through brain-derived neurotrophic factor signaling in microglial cells

Lai, Sheng-Wei, Chen, Jia-Hong, Lin, Hsiao-Yun, Liu, Yu-Shu, Tsai, Cheng-Fang, Chang, Pei-Chun, Lu, Dah-Yuu, Lin, Chingju·2018·Molecular Neurobiology
DOI 10.1007/s12035-018-0933-z
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Abstract

Inhibition of microglial over-activation is an important strategy to counter balance neurodegenerative progression. We previously demonstrated that the adenosine monophosphate-activated protein kinase (AMPK) may be a therapeutic target in mediating anti-neuroinflammatory responses in microglia. Brain-derived neurotrophic factor (BDNF) is one of the major neurotrophic factors produced by astrocytes to maintain the development and survival of neurons in the brain, and have recently been shown to modulate homeostasis of neuroinflammation. Therefore, the present study focused on BDNF-mediated neuroinflammatory responses and may provide an endogenous regulation of neuroinflammation. Among the tested neuroinflammation, epigallocatechin gallate (EGCG) and minocycline exerted BDNF upregulation to inhibit COX-2 and proinflammatory mediator expressions. Furthermore, both EGCG and minocycline upregulated BDNF expression in microglia through AMPK signaling. In addition, minocycline and EGCG also increased expressions of erythropoietin (EPO) and sonic hedgehog (Shh). In the endogenous modulation of neuroinflammation, astrocyte-conditioned medium (AgCM) also decreased the expression of COX-2 and upregulated BDNF expression in microglia. The anti-inflammatory effects of BDNF were mediated through EPO/Shh in microglia. Our results indicated that the BDNF-EPO-Shh novel-signaling pathway underlies the regulation of inflammatory responses and may be regarded as a potential therapeutic target in…

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Crossref · 10.1007/s12035-018-0933-z

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  • BDNF activates neuronal TrkB that regulates synaptic plasticity and modulates glutamatergic synaptic transmission in vivo and neuronal LTP.

    “BDNF has been shown to activate neuronal Tropomyosin-related kinase receptor B (TrkB) that regulates synaptic plasticity and modulate glutamatergic synaptic transmission in vivo and neuronal LTP, which is a key feature of memory formation and consolidation (Parkhurst et al., 2013; Lai et al., 2018).”

    From miR-142-3p Regulates BDNF Expression in Activated Rodent Microglia Through Its Target CAMK2A (2020) · cites this paper as Lai et al., 2018

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Authors
Lai, S.-W., Chen, J.-H., Lin, H.-Y., Liu, Y.-S., Tsai, C.-F., Chang, P.-C., Lu, D.-Y., & Lin, C.
ORCID
Lu, Dah-Yuu
Venue
Molecular Neurobiology
Publisher
Springer Science and Business Media LLC
Published
2018-02-09
Volume
55
Issue
9
Pages
7487-7499
ISSN
  • 0893-7648
  • 1559-1182
DOI
10.1007/s12035-018-0933-z
Cited by
80
References
6
Language
en
Licence
www.springer.com/tdm (tdm)
Funders
  • Ministry of Science and Technology, Taiwan (102-2320-B-039 -026 -MY3)
  • China Medical University (CMU105-AWARD-01)
  • Taichung Tzu Chi Hospital (TTCRD104-13)
  • Taiwan Ministry of Health and Welfare Clinical Trial and Research Center of Excellence (MOHW106-TDU-B-212-113004)

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