PlexinA1-deficient mice exhibit decreased cell density and augmented oxidative stress in parvalbumin-expressing interneurons in the medial prefrontal cortex

Jahan, Mst Sharifa; Tsuzuki, Takamasa; Ito, Takuji; Bhuiyan, M. K. J.; Takahashi, Ikuko; Takamatsu, Hyota; Kumanogoh, Atsushi; Negishi, Takayuki; Yukawa, Kazunori

doi:10.1016/j.ibneur.2022.11.002

Cited by 4 publications

(2 citation statements)

References 79 publications

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“…Several lines of evidence suggest a possible involvement of oxidative stress in schizophrenia pathogenesis in terms of both abnormal brain development [ 77 ] and peri/postnatal neurotoxic damage [ 26 ]. Antipsychotics are the mainstay of schizophrenia pharmacological treatment [ 325 ], and their mechanisms of action have been demonstrated to putatively intercept a few of the factors believed relevant for the onset or progression of the disease, including the oxidative balance [ 326 ]. Alterations in oxidative stress impair the regulation of the release of major neurotransmitters implicated in the disorder, above all dopamine [ 327 ] and glutamate [ 58 ], and their intracellular signaling both at cortical and subcortical levels [ 107 , 108 , 109 ], as well as the modification of the synapse structure and function [ 58 ].…”

Section: Discussionmentioning

confidence: 99%

Schizophrenia Synaptic Pathology and Antipsychotic Treatment in the Framework of Oxidative and Mitochondrial Dysfunction: Translational Highlights for the Clinics and Treatment

et al. 2023

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Schizophrenia is a worldwide mental illness characterized by alterations at dopaminergic and glutamatergic synapses resulting in global dysconnectivity within and between brain networks. Impairments in inflammatory processes, mitochondrial functions, energy expenditure, and oxidative stress have been extensively associated with schizophrenia pathophysiology. Antipsychotics, the mainstay of schizophrenia pharmacological treatment and all sharing the common feature of dopamine D2 receptor occupancy, may affect antioxidant pathways as well as mitochondrial protein levels and gene expression. Here, we systematically reviewed the available evidence on antioxidants’ mechanisms in antipsychotic action and the impact of first- and second-generation compounds on mitochondrial functions and oxidative stress. We further focused on clinical trials addressing the efficacy and tolerability of antioxidants as an augmentation strategy of antipsychotic treatment. EMBASE, Scopus, and Medline/PubMed databases were interrogated. The selection process was conducted in respect of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) criteria. Several mitochondrial proteins involved in cell viability, energy metabolism, and regulation of oxidative systems were reported to be significantly modified by antipsychotic treatment with differences between first- and second-generation drugs. Finally, antioxidants may affect cognitive and psychotic symptoms in patients with schizophrenia, and although the evidence is only preliminary, the results indicate that further studies are warranted.

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Section: Discussionmentioning

confidence: 99%

Schizophrenia Synaptic Pathology and Antipsychotic Treatment in the Framework of Oxidative and Mitochondrial Dysfunction: Translational Highlights for the Clinics and Treatment

et al. 2023

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“…The most novel nding was that the regulation of MICAL1 expression was strongly dependent on PlexinA1. MICAL1 was identi ed as an effector that took part in PlexinA1 signaling pathway for axon guidance (Jahan et al, 2022). MICAL1 can also mediate sema3a-induced Factin collapse, thereby regulating shape changes of podocyte in diabetic mice (Aggarwal et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

MICAL1 stability by PlexinA1 promotes gastric cancer cell migration

ye,

Xia,

Wang

et al. 2023

Preprint

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Background For metastasis to proceed, tumor cells must become mobile by modulating their cytoskeleton. MICAL1 is known as an actin cytoskeleton regulator, but the mechanisms by which it drives cancer cell migration are still unclear. Methods Immunohistochemistry assays and western blotting were used to detect the expression levels of MICAL1 in gastric cancer tissues and cells. Immunoprecipitation and immunofluorescence staining were used to detect the interactions of proteins. Wound-healing and transwell assays were performed to demonstrate the migratory function of MICAL1 in gastric cancer cells. In addition, qPCR, bioinformatics analysis, pulldown assay, ROS detection as well as western blotting were conducted to verify the mechanism of MICAL1 in gastric cancer cell migration. Results Analysis of gastric cancer tissues revealed that MICAL1 are elevated in gastric cancer tissues compared with non-tumor tissues and that its high expression is predictive of poor survival. PlexinA1 and MICAL1 were directly interact with each other. Specific inhibition of PlexinA1 accelerated MICAL1 ubiquitination and proteasome-based degradation. Furthermore, PlexinA1 positively regulates MICAL1 expression via Rac1 activation and following ROS production. Functional studies confirmed that PlexinA1 and MICAL1 facilitated gastric cancer cell migration via promoting vimentin expression. Conclusions These results indicate that PlexinA1 is a key regulator of MICAL1 stability via a Rac1/ROS dependent manner, and MICAL1 stability may be involved in promoting vimentin expression and gastric cancer cell migration.

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PlexinA1 promotes gastric cancer migration through preventing MICAL1 protein ubiquitin/proteasome-mediated degradation in a Rac1-dependent manner

Ye,

Xia,

Zhao

et al. 2024

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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PlexinA1-deficient mice exhibit decreased cell density and augmented oxidative stress in parvalbumin-expressing interneurons in the medial prefrontal cortex

Cited by 4 publications

References 79 publications

Schizophrenia Synaptic Pathology and Antipsychotic Treatment in the Framework of Oxidative and Mitochondrial Dysfunction: Translational Highlights for the Clinics and Treatment

Schizophrenia Synaptic Pathology and Antipsychotic Treatment in the Framework of Oxidative and Mitochondrial Dysfunction: Translational Highlights for the Clinics and Treatment

MICAL1 stability by PlexinA1 promotes gastric cancer cell migration

PlexinA1 promotes gastric cancer migration through preventing MICAL1 protein ubiquitin/proteasome-mediated degradation in a Rac1-dependent manner

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