Nerve growth factor (NGF) expression in rat microglia is induced by adenosine A2a-receptors
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Acknowledgements
This study was supported by the Swiss National Foundation for Scientific Research (Grant 3100-049397.96-1), by Deutsche Forschungsgesellschaft (SFB 505/B1, B5 and Li643/2-1) and by Bundesministerium für Forschung und Technologie/BMFT (Grant 01 KL 9303/1).
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2020, Pharmacological ResearchCitation Excerpt :Although this effect is only evident when glutamatergic excitotoxicity is present [434,435], which is the case of most brain disorders [60,61], whereas upon acute infection A2ARs have an opposite effect on neuroinflammation (e.g. [435–439] as previously reviewed in detail [440]). Microglial A2AR activation also triggers trophic effects, as heralded by the observations that the activation of A2ARs in a microglial cell line engage the cAMP-PKA signaling to trigger brain-derived neurotrophic factor (BDNF) release that bolsters for microglia proliferation [395,441] and also up-regulate and release of nerve growth factor (NGF), a neurotrophic factor that promotes neuronal regeneration [442]. These A2AR-generated trophic factors might be associated with the sex-dependent and brain-region-dependent asymmetric maturation of microglia during development [443–445].
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2020, Journal of the Neurological SciencesCitation Excerpt :The use of the A2A receptor antagonist, SCH58261, reduces p38 phosphorylation in microglia which results in attenuation of hippocampus damage post-OGD, reduction of infarction volume and improvement of prognosis [91,125,126]. In addition, studies have shown that the activation of central microglia A2A receptors increases the expression and release of NGF [127–129]. Activation of the A3 receptor prevents infiltration and migration of microglia or monocytes into the cerebral ischemic area [130] and attenuates inflammatory damage caused by cerebral ischemic injury.
Purinergic signalling in brain ischemia
2016, NeuropharmacologyLow doses of the selective adenosine A<inf>2A</inf> receptor agonist CGS21680 are protective in a rat model of transient cerebral ischemia
2014, Brain ResearchCitation Excerpt :In our study, we cannot however exclude that adenosine A2A receptor agonists exert a role in brain ischemia also acting on central A2A receptors. Activation of central A2A receptors is known to increase expression and release of neurotrophic factors (Sebastião and Ribeiro, 2009) such as NGF from microglia (Heese et al., 1997), BDNF from mice hippocampal neurons (Tebano et al., 2008) and from rat cortical neurons (Jeon et al., 2011). Therefore, the increased expression of neurotrophic factor(s) by adenosine A2A receptor stimulation may contribute to restore neurological functions and cerebral damage after brain ischemia.
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2014, International Review of NeurobiologyCitation Excerpt :However, it cannot be excluded that adenosine A2A receptor agonists display protection against brain ischemia also by direct effects on central A2A receptors. Activation of central A2A receptors is known to increase expression and release of neurotrophic factors (Sebastião & Ribeiro, 2009) as NGF in microglia (Heese, Fiebich, Bauer, & Otten, 1997) and BDNF in mice hippocampus (Tebano et al., 2008) and in rat cortical neurons (Jeon et al., 2011). The increase in neurotrophic factor expression by adenosine A2A receptor stimulation may contribute to restore neurological functions and cerebral damage after brain ischemia (Ke, Xiong, & Liu, 2012).