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LncRNA ENST00000581911 regulates extraocular muscle remodeling by interacting with KHSRP in Graves’ ophthalmopathy

ABSTRACT: LncRNA ENST00000581911 regulates extraocular muscle remodeling by interacting with KHSRP in Graves’ ophthalmopathy

PROVIDER: PRJNA1169784 | ENA |

REPOSITORIES: ENA

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LncRNA ENST00000581911 regulates extraocular muscle remodeling by interacting with KHSRP in Graves’ ophthalmopathy

Project description:To reveal the potential role of lncRNAs in the extraocular muscles (EOMs) of Graves' ophthalmopathy (GO), we performed lncRNA expression profiling and compared their expression differences between EOM tissues sampled from GO and concomitant esotropia (CET) patients using microarray analysis. To reveal the potential role of lncRNAs in the extraocular muscles (EOMs) of Graves' ophthalmopathy (GO), we performed lncRNA expression profiling and compared their expression differences between EOM tissues sampled from GO and concomitant esotropia (CET) patients using microarray analysis.

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Project description:By studying the differences in transcriptional and methylation levels between the GO (Graves' ophthalmopathy) patient group and the GH (Graves' hyperthyroidism) patient group, we aim to explore the pathogenic mechanisms of GO in patients with GH, and provide intervention guidance for the prevention of GO.

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The cardiac calsequestrin gene (CASQ2) is up-regulated in the thyroid in patients with Graves’ ophthalmopathy

Project description:Thyroid-associated ophthalmopathy (TAO) is a complex eye and orbital disorder that is uniquely linked to Graves’ hyperthyroidism (GH). A popular explanation for the development of orbital inflammation in these patients is autoimmunity against the TSH-receptor expressed in orbital preadipocytes. However, this has not been proven and alternative hypotheses should be entertained. We have shown recently that antibodies against highly purified rabbit skeletal muscle calsequestrin are sensitive and specific markers of eye muscle inflammation in patients with thyroid autoimmunity. Keywords: disease state comparison In the study presented here, RNA from thyroid tissue of hyperthyroid patients with (n=10) and without (n=8) symptoms of ophthalmopathy was compared across 20,589 genes.

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Homo sapiens

Project description:LncRNA ENST00000581911 regulates extraocular muscle remodeling by interacting with KHSRP in Graves' ophthalmopathy

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The cardiac calsequestrin gene (CASQ2) is up-regulated in the thyroid in patients with Graves’ ophthalmopathy

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Dihydroartemisinin Exerts Antifibrotic and Anti-inflammatory Effects in Graves’ Ophthalmopathy by Targeting Orbital Fibroblasts

Project description:Graves’ ophthalmopathy (GO) is a common orbital disease that threatens visual function and appearance. Orbital fibroblasts (OFs) are considered key target and effector cells in GO. In addition, hyaluronan (HA) production, inflammation, and orbital fibrosis are intimately linked to the pathogenesis of GO. In this study, we explored the therapeutic effects of dihydroartemisinin (DHA), an antimalarial drug, on GO-derived, primary OFs. RNA sequencing was conducted to identify differentially expressed genes (DEGs) in DHA-treated OFs, and Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of DEGs was performed to explore potential mechanisms mediating the antifibrotic effect of DHA on GO-derived OFs. Results showed that DHA dose-dependently inhibited OF proliferation and downregulated, at the mRNA and protein levels, TGF-β1-induced expression of fibrosis markers, including alpha smooth muscle actin (α-SMA) and connective tissue growth factor (CTGF). Furthermore, DHA inhibited TGF-β1 induced phosphorylation of extracellular signal-regulated protein kinase 1/2 (ERK1/2) and signal transducer and activator of transcription 3 (STAT3), which suggested that DHA exerted antifibrotic effects via suppression of the ERK and STAT3 signaling pathways.In conclusion, our study provides first-time evidence that DHA may significantly alleviate pathogenic manifestations of GO by inhibiting proliferation, fibrosis- and inflammation-related gene expression, and HA production in OFs. These data suggest that DHA may be a promising candidate drug for treatment of GO.

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