Schwann cells protect against CaMKII- and PKA-dependent Acrylamide-induced Synapsin I phosphorylation

Chen, Xiao; Wang, Xiuhui; Yang, Yiguang; Li, Zhongsheng; Zhang, Yi; Gao, Weimin; Xiao, Jingwei; B, Li

doi:10.1016/j.brainres.2018.07.019

Cited by 4 publications

(2 citation statements)

References 40 publications

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“…ERK phosphorylates mammalian synapsin I at positions 4 and 5 of domain B and at position 6 of domain D (57). In addition, PKA and CaMKII can also act by phosphorylating synapsin I (58). In this study, a decrease was observed in the level of p-synapsin Ia/b (Ser549) after CMB model creation.…”

Section: Discussionmentioning

confidence: 50%

Cystatin C promotes cognitive dysfunction in rats with cerebral microbleeds by inhibiting the ERK/synapsin Ia/Ib pathway

Sun

et al. 2019

Exp Ther Med

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Although higher serum level of cystatin C (CysC) was observed in patients with cerebral microbleeds, its associated role in the disease has not been elucidated. In this work, a rat model of cerebral microbleeds was created with the aim of investigating effects of CysC on cognitive function in rats with cerebral microbleeds and the underlying mechanism. Serum samples of patients with cerebral microbleeds and healthy people of the same age were collected. Levels of cystatin C expression in these samples were measured using CysC kits. Moreover, 48 spontaneously hypertensive rats (SHRs) bred under specific pathogen-free (SPF) conditions were randomly divided into 4 groups: sham surgery control group (sham), model group (CMB), model + empty vector control group (CMB + vehicle), and model + cystatin C overexpression group (CMB + CysC). Expression levels of CysC in hippocampus of rats in each group were measured by western blot analysis. The Y-maze was used to evaluate cognitive function of rats. Hippocampal long-term potentiation (LTP) in rats was assessed by the electrophysiological assay. Alterations in levels of p-ERK1/2 and p-synapsin Ia/b proteins associated with cognitive function were identified by western blot analysis. The serum levels of CysC in patients with cerebral microbleeds were significantly upregulated (P<0.001). After injection of CysC, its expression levels in rat hippocampus were significantly increased (P<0.001), which enhanced the decline in learning and memory function, as well as the decrease of LTP in the rat model of cerebral microbleeds (P<0.001). Western blot results showed that injection of CysC further reduced the levels of p-ERK1/2 and p-synapsin Ia/b in the rat model of microbleeds (P<0.001). CysC was up regulated in serum of patients with cerebral microbleeds. It promoted cognitive dysfunction in rats with microbleeds by inhibiting ERK/synapsin Ia/Ib pathway.

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Section: Discussionmentioning

confidence: 50%

Cystatin C promotes cognitive dysfunction in rats with cerebral microbleeds by inhibiting the ERK/synapsin Ia/Ib pathway

Sun

et al. 2019

Exp Ther Med

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“…4 Subchronic exposure to acrylamide causes sensory, motor and autonomic dysfunctions such as ataxia, gait abnormalities, skeletal muscle weakness and numbness of hands and feet. 5,6 Given the exposure to acrylamide is inevitable, it is crucial to search new treatment strategies for the repair of acrylamide-induced nerve injury and functional reconstruction.…”

Section: Introductionmentioning

confidence: 99%

The effects of acrylamide-mediated dorsal root ganglion neurons injury on ferroptosis

Shi

Liu

et al. 2022

Hum Exp Toxicol

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Acrylamide (ACR) is a water-soluble chemical applied in industrial and laboratory processes. The neurotoxicity induced by acrylamide involves both peripheral and central nervous system. Hence, there is a growing urgency to investigate the mechanisms of acrylamide-induced neurotoxicity and search novel therapeutic target for the nerve repair. The effects of ACR on the proliferation, reactive oxygen species (ROS) and iron production of dorsal root ganglia (DRG) neurons and Schwann cells were determined. 5-Ethynyl-2′-deoxyuridine (EDU) staining and transwell assay were applied to detect the proliferation and migration capacity of DRG cells. Ferrostatin-1 (Fer-1) was used to suppress ferroptosis induced by ACR. RT-PCR analysis was performed to examine the expression of neurotrophic factors including brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), vascular endothelial growth factor (VEGF) and glial cell line-derived neurotrophic factor (GDNF). Moreover, Iron, ROS, malondialdehyde (MDA) and glutathione (GSH) contents were measured to reveal the regulation of ferroptosis in ACR-related nerve injury. ACR inhibited the proliferation and migration of DRG neurons and the supplementation of Fer-1 reversed the effects induced by ACR. Besides, the treatment of Fer-1 effectively increased the expression of NGF, BDNF, VEGF and GDNF. Furthermore, ACR increased the iron level, MDA and ROS contents while inhibited the level of GSH. It was unveiled that ACR attenuated the proliferation, migration and neuron repair of DRG neurons through regulating ferroptosis. The modulation of ferroptosis might be a promising therapeutic strategy and provide references for future treatment of acrylamide-induced nerve damage.

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Acrylamide-induced damage to postsynaptic plasticity is CYP2E1 dependent in an SH-SY5Y co-culture system

Chen

Xiao²,

Hao³

et al. 2022

Toxicology in Vitro

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Schwann cells protect against CaMKII- and PKA-dependent Acrylamide-induced Synapsin I phosphorylation

Cited by 4 publications

References 40 publications

Cystatin C promotes cognitive dysfunction in rats with cerebral microbleeds by inhibiting the ERK/synapsin Ia/Ib pathway

Cystatin C promotes cognitive dysfunction in rats with cerebral microbleeds by inhibiting the ERK/synapsin Ia/Ib pathway

The effects of acrylamide-mediated dorsal root ganglion neurons injury on ferroptosis

Acrylamide-induced damage to postsynaptic plasticity is CYP2E1 dependent in an SH-SY5Y co-culture system

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