Astrocyte truncated tropomyosin receptor kinase B mediates brain‐derived neurotrophic factor anti‐apoptotic effect leading to neuroprotection

Saba, Julieta; Turati, Juan; Ramírez, Delia; Carniglia, Lila; Durand, Daniela Elizabeth; Lasaga, Mercedes; Caruso, Carla Mariana

doi:10.1111/jnc.14476

Cited by 54 publications

(40 citation statements)

References 72 publications

(168 reference statements)

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“…Given that γ‐GCL activity is regulated at multiple levels, it is possible that PA affects transcriptional activity, whereas NDP‐MSH induces post‐transcriptional changes. Moreover, we recently reported that BDNF induces GSH synthesis in astrocytes and, in the present study, we show that NDP‐MSH prevented the reduction in BDNF expression induced by PA, suggesting that BDNF could be a mediator of NDP‐MSH antioxidant effect in astrocytes.…”

Section: Discussionsupporting

confidence: 76%

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NDP‐MSH reduces oxidative damage induced by palmitic acid in primary astrocytes

Ramírez

Saba

Turati

et al. 2019

J Neuroendocrinology

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Recent findings relate obesity to inflammation in key hypothalamic areas for body weight control. Hypothalamic inflammation has also been related to oxidative stress.Palmitic acid (PA) is the most abundant free fatty acid found in food, and in vitro studies indicate that it triggers a pro-inflammatory response in the brain.Melanocortins are neuropeptides with proven anti-inflammatory and neuroprotective action mediated by melanocortin receptor 4 (MC4R), but little is known about the effect of melanocortins on oxidative stress. The aim of this study was to investigate whether melanocortins could alleviate oxidative stress induced by a high fat diet (HFD) model. We found that NDP-MSH treatment decreased PA-induced reactive oxygen species production in astrocytes, an effect blocked by the MC4R inhibitor JKC363. NDP-MSH abolished nuclear translocation of Nrf2 induced by PA and blocked the inhibitory effect of PA on superoxide dismutase (SOD) activity and glutathione levels while it also per se increased activity of SOD and γ-glutamate cysteine ligase (γ-GCL) antioxidant enzymes. However, HFD reduced hypothalamic MC4R and brain derived neurotrophic factor mRNA levels, thereby preventing the neuroprotective mechanism induced by melanocortins. K E Y W O R D Sastrocytes, high-fat diet, MC4R, oxidative stress, palmitic acid

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Section: Discussionsupporting

confidence: 76%

“…Intracellular ROS levels were detected using 2′‐7′‐dichlorofluorescein diacetate (DCFH‐DA) which, when hydrolysed within the cell, is oxidised to fluorescent dichlorofluorescein, as described by Saba et al . Cells were seeded onto 96‐well plates at a density of 3 × 10 4 cells per well.…”

Section: Methodsmentioning

confidence: 99%

NDP‐MSH reduces oxidative damage induced by palmitic acid in primary astrocytes

Ramírez

Saba

Turati

et al. 2019

J Neuroendocrinology

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“…However, little is known about the role of BDNF in astrocytes. A previous study reported that BDNF delivery stimulated astrocytes to release neuroprotective factors, contributing to neuronal survival in the CNS (Saba et al, ), and the production of these neurotrophic factors was attenuated in GFAP‐specific TrkB knockout mice (Harada et al, ), indicating that the induction of neurotrophic factors in astrocytes could be triggered by activation of the BDNF/TrkB signalling pathway.…”

Section: Discussionmentioning

confidence: 99%

Neurotrophic interactions between neurons and astrocytes following AAV1‐Rheb(S16H) transduction in the hippocampus in vivo

Jeon

Moon

Kim

et al. 2019

British J Pharmacology

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Background and Purpose: We recently reported that AAV1-Rheb(S16H) transduction could protect hippocampal neurons through the induction of brain-derived neurotrophic factor (BDNF) in the rat hippocampus in vivo. It is still unclear how neuronal BDNF produced by AAV1-Rheb(S16H) transduction induces neuroprotective effects in the hippocampus and whether its up-regulation contributes to the enhance of a neuroprotective system in the adult brain. ---This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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“…To confirm the effect of surgical incision-induced nociception on BDNF signaling pathway activation, ANA-12 was used to block the combination of BDNF and TrkB. 26 ANA-12 attenuated the increase in pTrkB and improvement in fear learning ability induced by surgical stimuli blockade. These data suggested that plantar incision-induced nociception decreased fear learning function by inhibiting the BDNF signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Surgical incision induces learning impairment in mice partially through inhibition of the brain-derived neurotrophic factor signaling pathway in the hippocampus and amygdala

Liu

et al. 2018

Mol Pain

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Surgical incision-induced nociception contributes to the occurrence of postoperative cognitive dysfunction. However, the exact mechanisms involved remain unclear. Brain-derived neurotrophic factor (BDNF) has been demonstrated to improve fear learning ability. In addition, BDNF expression is influenced by the peripheral nociceptive stimulation. Therefore, we hypothesized that surgical incision-induced nociception may cause learning impairment by inhibiting the BDNF/tropomyosin-related kinase B (TrkB) signaling pathway. The fear conditioning test, enzyme-linked immunosorbent assay, and Western blot analyses were used to confirm our hypothesis and determine the effect of a plantar incision on the fear learning and the BDNF/TrkB signaling pathway in the hippocampus and amygdala. The freezing times in the context test and the tone test were decreased after the plantar incision. A eutectic mixture of local anesthetics attenuated plantar incision-induced postoperative pain and fear learning impairment. ANA-12, a selective TrkB antagonist, abolished the improvement in fear learning and the activation of the BDNF signaling pathway induced by eutectic mixture of local anesthetics. Based on these results, surgical incision-induced postoperative pain, which was attenuated by postoperative analgesia, caused learning impairment in mice partially by inhibiting the BDNF signaling pathway. These findings provide insights into the mechanism underlying surgical incision-induced postoperative cognitive function impairment.

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Astrocyte truncated tropomyosin receptor kinase B mediates brain‐derived neurotrophic factor anti‐apoptotic effect leading to neuroprotection

Abstract: Open Science: This manuscript was awarded with the Open Materials Badge. For more information see: https://cos.io/our-services/open-science-badges/.

Cited by 54 publications

References 72 publications

NDP‐MSH reduces oxidative damage induced by palmitic acid in primary astrocytes

NDP‐MSH reduces oxidative damage induced by palmitic acid in primary astrocytes

Neurotrophic interactions between neurons and astrocytes following AAV1‐Rheb(S16H) transduction in the hippocampus in vivo

Surgical incision induces learning impairment in mice partially through inhibition of the brain-derived neurotrophic factor signaling pathway in the hippocampus and amygdala

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