14,15‐epoxyeicosatrienoic acid produced by cytochrome P450s enhances neurite outgrowth of <scp>PC</scp>12 and rat hippocampal neuronal cells

Oguro, Ami; Inoue, Takumi; Kudoh, Suguru N.; Imaoka, Shingi

doi:10.1002/prp2.428

Cited by 11 publications

(4 citation statements)

References 55 publications

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“…Consequently, blockade of BDNF-TrkB signaling ablates the protective effect of sEH genetic deletion in middle cerebral arterial occlusion (MCAO) models of stroke [31,32]. In addition to the protective effects of EETs through their actions on auxiliary cells, EETs are directly able to elicit effects in neurons including growth of neurites [34,35]. These effects suggest sEH inhibition may reduce CNS injury both by reducing the inflammatory response in resident immune cells and by direct neuro-protective effects on the neurons.…”

Section: Neuro-inflammation Induced By Acute Injurymentioning

confidence: 99%

Role of epoxy-fatty acids and epoxide hydrolases in the pathology of neuro-inflammation

Kodani

Morisseau

2019

Biochimie

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Neuroinflammation is a physiologic response aimed at protecting the central nervous system during injury. However, unresolved and chronic neuroinflammation can lead to long term damage and eventually neurologic disease including Parkinson's disease, Alzheimer's disease and dementia. Recently, enhancing the concentration of epoxyeicosatrienoic acids (EETs) through blocking their hydrolytic degradation by soluble epoxide hydrolase (sEH) has been applied towards reducing the long-term damage associated with central neurologic insults. Evidence suggests this protective effect is mediated, at least in part, through polarization of microglia to an anti-inflammatory phenotype that blocks the inflammatory actions of prostaglandins and promotes wound repair. This mini-review overviews the epidemiologic basis for using sEH inhibition towards neuroinflammatory disease and pharmacologic studies testing sEH inhibition in several neurologic diseases. Additionally, the combination of sEH inhibition with other eicosanoid signaling pathways is considered as an enhanced approach for developing potent neuroprotectants.

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Section: Neuro-inflammation Induced By Acute Injurymentioning

confidence: 99%

Role of epoxy-fatty acids and epoxide hydrolases in the pathology of neuro-inflammation

Kodani

Morisseau

2019

Biochimie

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“…A lipid precursor, arachidonic acid (AA) can be metabolized into families of biologically active mediators through CYP450 pathway 23,24 . It has been confirmed that various cytochromase P450 were involved in the metabolic process of epoxyeicosatrienoic acid (EET) generated from AA 25 . EET can also reduce the up‐regulation of endothelial cell adhesion molecule induced by cytokines, inhibit the adhesion of lymphocyte to blood vessels, the activation of nuclear factor (NF‐κB) and inhibit the activation of monocyte/macrophage and its subsequent cascade reaction.…”

Section: Discussionmentioning

confidence: 99%

Association between CYP2C19 gene polymorphisms and susceptibility to high‐altitude pulmonary edema

Bai

Guan

et al. 2020

Clinical Respiratory J

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High-altitude pulmonary edema (HAPE) is a noncardiogenic form of pulmonary edema, which often occurs in those who enter the plateau for the first time or re-enter the plateau. When people quickly enter the area with an altitude of more than 3000 m, but cannot adapt to the altitude hypobaric hypoxia environment, resulting in abnormal pulmonary function and complications. 1,2 Early symptoms of HAPE include cough, dyspnea and decreased motor ability. Gradually, cough worsens, breathing becomes difficult to rest and even hard to breathe. 3,4 The development of HAPE has been associated with rate of ascent, high altitude, importantly, individual susceptibility are the major factors that contribute to high-altitude maladies. 5 Basnyat et al reported a 5% incidence of HAPE in 228 pilgrims climbed from 2000 m to 4300 m a day at Langtang in Nepal. 6 Of the Indian soldiers transported to 3500 m in Kashmir, 5.7% will develop HAPE during flight. 7 Up to now, a larger study was to assess HAPE involved 3628 Chinese soldiers

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“…Several studies have shown that 14,15-EET can induce secretion of vascular endothelial growth factor (VEGF) and BDNF to protect the existing neurons during inflammation [ 176 , 216 ]. Apart from the protective effects of EETs through their actions on auxiliary cells, EETs can directly impact neurons, for instance, by enhancing their neurite outgrowth [ 123 , 143 , 178 , 217 ]. In addition, both genetic ablation and pharmacological inhibition of sEH could attenuate the functional and historical deficits in cerebral ischemia by vascular and neural protection [ 218 , 219 ].…”

Section: Ep-pufas and Neuroinflammationmentioning

confidence: 99%

Cytochrome P450 Metabolism of Polyunsaturated Fatty Acids and Neurodegeneration

et al. 2020

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Due to the aging population in the world, neurodegenerative diseases have become a serious public health issue that greatly impacts patients’ quality of life and adds a huge economic burden. Even after decades of research, there is no effective curative treatment for neurodegenerative diseases. Polyunsaturated fatty acids (PUFAs) have become an emerging dietary medical intervention for health maintenance and treatment of diseases, including neurodegenerative diseases. Recent research demonstrated that the oxidized metabolites, particularly the cytochrome P450 (CYP) metabolites, of PUFAs are beneficial to several neurodegenerative diseases, including Alzheimer’s disease and Parkinson’s disease; however, their mechanism(s) remains unclear. The endogenous levels of CYP metabolites are greatly affected by our diet, endogenous synthesis, and the downstream metabolism. While the activity of omega-3 (ω-3) CYP PUFA metabolites and omega-6 (ω-6) CYP PUFA metabolites largely overlap, the ω-3 CYP PUFA metabolites are more active in general. In this review, we will briefly summarize recent findings regarding the biosynthesis and metabolism of CYP PUFA metabolites. We will also discuss the potential mechanism(s) of CYP PUFA metabolites in neurodegeneration, which will ultimately improve our understanding of how PUFAs affect neurodegeneration and may identify potential drug targets for neurodegenerative diseases.

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14,15‐epoxyeicosatrienoic acid produced by cytochrome P450s enhances neurite outgrowth of PC12 and rat hippocampal neuronal cells

Cited by 11 publications

References 55 publications

Role of epoxy-fatty acids and epoxide hydrolases in the pathology of neuro-inflammation

Role of epoxy-fatty acids and epoxide hydrolases in the pathology of neuro-inflammation

Association between CYP2C19 gene polymorphisms and susceptibility to high‐altitude pulmonary edema

Cytochrome P450 Metabolism of Polyunsaturated Fatty Acids and Neurodegeneration

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