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Epigenetic alterations of the imprinted SLC22A18 gene contributed to congenital "Allergy-Short-stature-fatty liver" syndrome by via β-catenin-Ascl2 axis

ABSTRACT: Epigenetic syndrome is a multisystem, eternal, and devastating disease associated with imprinted gene variants. Our previous study showed a strong correlation between the SLC22A18 and the "Allergy-Short stature-fatty liver" (ASFL) syndrome in children. However, the mechanisms by which SLC22A18 influences ASFL syndrome remain unknown.SLC22A18 deficiency also induced higher lipid accumulation in liver in the mouse model. Whether SLC22A18 deletion promotes hepatic steatosis deserves further investigation.

ORGANISM(S): Mus musculus

PROVIDER: GSE322487 | GEO | 2026/03/05

REPOSITORIES: GEO

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Project description:Background: The prevalence of individuals allergic to latex, exhibiting cross-hypersensitivity with plant-derived food has been frequently reported as the so-called latex-fruit syndrome. Nonetheless, molecular mechanisms underlying allergy to latex and/or fruit are poorly understood. Objective: The aims of this study were to identify candidate genes that may be associated with the pathogenesis of allergy to latex and /or vegetable food, and to assess if similar molecular pathways are involved in both types of hypersensitivity. Methods: DNA microarray analysis was performed to screen the molecular profiles of peripheral blood mononuclear cells isolated from patients with allergy to latex, to fruit, or with latex-fruit syndrome, and from control healthy subjects. Results: Gene expression profiling identified an overlapping dataset of genes commonly regulated in all the atopic patients enrolled in this study, suggesting that similar molecular mechanisms are involved in the pathogenesis of allergy to the fruit and /or latex. Several regulators of the innate and acquired immunity reported to polarize the immunological response towards a Th2-mediated immune response were overexpressed in patients. Furthermore, evidences suggested that T regulatory cell expression might be defective in allergic patients, as a consequence of a dysregulation of some inflammatory cytokines. Finally, several transcription factors that may be responsible for the Th1/Th2 imbalance were modulated in allergic patients. Conclusion and clinical implications: This study identified relevant genes that may help to elucidate the molecular mechanisms underlying allergic disease. Knowledges of critical targets, along with transcription factors regulating gene activity may facilitate the development of new therapies. Experiment Overall Design: This study aimed at the understanding of the molecular pathways involved in allergy to latex and fruit. As latex and vegetable food allergens cross-react, it could be hypothesized that similar pathways are involved in both types of hypersensitivity. Experiment Overall Design: For this purpose, patients allergic to latex (n=6), allergic to vegetable food (n=5), or suffering from latex-fruit syndrome (n=6) were enrolled from the Unit of Allergy of the Gemelli Hospital of Rome. Moreover, 4 healthy volunteers were added to this study. Five ml of blood were harvested from each individual, and PBMCs were isolated on ficoll gradient. Following sample preparation (as recommended by the manufacturer), each sample was hybridized on Affymetrix human focus array. Data were processed with Affymetrix MAS 5.0 software and averaged intensity of signals from biological replicates were calculated for further analysis. Experiment Overall Design: The CEL files for this study were lost in a computer crash.

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Epigenetic alterations of the imprinted SLC22A18 gene contributed to congenital "Allergy-Short-stature-fatty liver" syndrome by via β-catenin-Ascl2 axis

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