The Role of Prostaglandins in Autism
A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".
Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 4562
Special Issue Editor
Interests: autism; antioxidant protein; oxidtive stress; tuberous sclerosis; cell mechanism of signaling
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Dear Colleagues,
Prostaglandins are a series of unsaturated fatty acids that play critical roles in regulating various neuronal signals. Endoperoxide H synthases-1/2 (cyclooxygenases-1/2, COX-1/2) catalyze the commitment step in prostaglandin synthesis. Moreover, prostaglandins (PGD2, PGE2, PGF2α), prostacyclin (PGI2), and thromboxane A2 (TXA2) form the prostanoid family of lipid mediators.
Alterations in their biosynthesis are accompanied by a wide range of pathological conditions. Prostaglandin E2 (PGE2) is a membrane-derived lipid signaling molecule that has an important role in neuronal development. Abnormal PGE2 function, possibly due to environmental insult during prenatal development, has been linked to brain pathologies such as autism spectrum disorder (ASD). PGE2 may destabilize the actin cytoskeleton at various stages of neuronal differentiation, causing changes in neuronal morphology. Moreover, PGE2 is a lipid signaling molecule important for brain development and function in neuronal cell lines. Prenatal exposure to PGE2 affects the Wnt pathway at the level of β-catenin, the major downstream regulator of Wnt-dependent gene transcription. After maternal exposure, PGE2 signaling converges with the Wnt canonical pathway in the developing mouse brain. All affected genes have been previously associated with disorders of the central nervous system, including ASD. Additionally, the addition of PGE2 to neuronal cells leads to changes in the expression of Wnt genes and the activation of non-phospho β-catenin abnormal PGE2 levels in the mouse brain during development, which may interfere with the Wnt pathway via the phosphorylation of β-catenin at multiple sites, leading to a differential expression of crucial neurodevelopmental genes.
Prostaglandin H synthases or cyclooxygenases (COX -1 and COX-2) play a central role in the inflammatory cascade by converting arachidonic acid into bioactive prostanoids, which is relevant to the pathophysiology of ASD. COX-2 activity is linked to anti-inflammatory and neuroprotective actions and is involved in the generation of novel lipid mediators with pro-resolution properties.
The investigation of links between the various types of prostaglandins, Wnt signaling, and the role of COX -1 and COX-2 are important issues in the pathophysiology of ASD.
Prof. Dr. Kunio Yui
Guest Editor
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Keywords
- autism spectrum disorder
- prostaglandins
- prostaglandin E2
- cyclooxygenases
- signaling mediator
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