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Circular RNA profile in Graves’ disease and potential function of hsa_circ_0090364

BACKGROUND: Graves’ disease is a common autoimmune disease. Cytokines and their signalling pathways play a major part in the pathogenesis of Graves’ disease; however, the underlying mechanism needs to be clarified. AIMS: The aim of this study was to explore whether circular RNAs participate in the i...

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Autores principales: Jiang, Zhengrong, Huang, Linghong, Chen, Lijun, Zhou, Jingxiong, Liang, Bo, Bai, Xuefeng, Wu, Lizhen, Huang, Huibin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Bioscientifica Ltd 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9578071/
https://www.ncbi.nlm.nih.gov/pubmed/36018563
http://dx.doi.org/10.1530/EC-22-0030
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author Jiang, Zhengrong
Huang, Linghong
Chen, Lijun
Zhou, Jingxiong
Liang, Bo
Bai, Xuefeng
Wu, Lizhen
Huang, Huibin
author_facet Jiang, Zhengrong
Huang, Linghong
Chen, Lijun
Zhou, Jingxiong
Liang, Bo
Bai, Xuefeng
Wu, Lizhen
Huang, Huibin
author_sort Jiang, Zhengrong
collection PubMed
description BACKGROUND: Graves’ disease is a common autoimmune disease. Cytokines and their signalling pathways play a major part in the pathogenesis of Graves’ disease; however, the underlying mechanism needs to be clarified. AIMS: The aim of this study was to explore whether circular RNAs participate in the immunological pathology of Graves’ disease via cytokine-related signalling pathways. METHODS: Bioinformatics analysis was performed to identify differentially expressed circular RNAs and their targets and associated pathways. A total of three patients with Graves’ disease and three sex- and age-matched healthy controls were enrolled for validation with microarray analysis and real-time quantitative PCR (qPCR). An additional 24 patients with Graves’ disease and 24 gender- and age-matched controls were included for validation by real-time fluorescent qPCR. Flow cytometry and CCK8 assays were used to detect the apoptotic and proliferative levels of Jurkat cells (T lymphocytes) with the silenced expression of circRNA. ELISA was performed to detect the growth and apoptosis-related proteins. The competition mechanism of endogenous RNA was explored by real-time fluorescence qPCR. RESULTS: A total of 366 significantly differentially expressed circular RNAs were identified in the Graves’ disease group compared to healthy controls. The level of hsa_circ_0090364 was elevated in Graves’ disease patients and positively correlated with thyroid-stimulating hormone receptor antibodies. Further analyses suggested that hsa_circ_0090364 may regulate the JAK-STAT pathway via the hsa-miR-378a-3p/IL-6ST/IL21R axis to promote cell growth. CONCLUSIONS: These results provide novel clues into the pathophysiological mechanisms of Graves’ disease and potential targets for drug treatment.
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spelling pubmed-95780712022-10-18 Circular RNA profile in Graves’ disease and potential function of hsa_circ_0090364 Jiang, Zhengrong Huang, Linghong Chen, Lijun Zhou, Jingxiong Liang, Bo Bai, Xuefeng Wu, Lizhen Huang, Huibin Endocr Connect Research BACKGROUND: Graves’ disease is a common autoimmune disease. Cytokines and their signalling pathways play a major part in the pathogenesis of Graves’ disease; however, the underlying mechanism needs to be clarified. AIMS: The aim of this study was to explore whether circular RNAs participate in the immunological pathology of Graves’ disease via cytokine-related signalling pathways. METHODS: Bioinformatics analysis was performed to identify differentially expressed circular RNAs and their targets and associated pathways. A total of three patients with Graves’ disease and three sex- and age-matched healthy controls were enrolled for validation with microarray analysis and real-time quantitative PCR (qPCR). An additional 24 patients with Graves’ disease and 24 gender- and age-matched controls were included for validation by real-time fluorescent qPCR. Flow cytometry and CCK8 assays were used to detect the apoptotic and proliferative levels of Jurkat cells (T lymphocytes) with the silenced expression of circRNA. ELISA was performed to detect the growth and apoptosis-related proteins. The competition mechanism of endogenous RNA was explored by real-time fluorescence qPCR. RESULTS: A total of 366 significantly differentially expressed circular RNAs were identified in the Graves’ disease group compared to healthy controls. The level of hsa_circ_0090364 was elevated in Graves’ disease patients and positively correlated with thyroid-stimulating hormone receptor antibodies. Further analyses suggested that hsa_circ_0090364 may regulate the JAK-STAT pathway via the hsa-miR-378a-3p/IL-6ST/IL21R axis to promote cell growth. CONCLUSIONS: These results provide novel clues into the pathophysiological mechanisms of Graves’ disease and potential targets for drug treatment. Bioscientifica Ltd 2022-09-28 /pmc/articles/PMC9578071/ /pubmed/36018563 http://dx.doi.org/10.1530/EC-22-0030 Text en © The authors https://creativecommons.org/licenses/by-nc/4.0/This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. (https://creativecommons.org/licenses/by-nc/4.0/)
spellingShingle Research
Jiang, Zhengrong
Huang, Linghong
Chen, Lijun
Zhou, Jingxiong
Liang, Bo
Bai, Xuefeng
Wu, Lizhen
Huang, Huibin
Circular RNA profile in Graves’ disease and potential function of hsa_circ_0090364
title Circular RNA profile in Graves’ disease and potential function of hsa_circ_0090364
title_full Circular RNA profile in Graves’ disease and potential function of hsa_circ_0090364
title_fullStr Circular RNA profile in Graves’ disease and potential function of hsa_circ_0090364
title_full_unstemmed Circular RNA profile in Graves’ disease and potential function of hsa_circ_0090364
title_short Circular RNA profile in Graves’ disease and potential function of hsa_circ_0090364
title_sort circular rna profile in graves’ disease and potential function of hsa_circ_0090364
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9578071/
https://www.ncbi.nlm.nih.gov/pubmed/36018563
http://dx.doi.org/10.1530/EC-22-0030
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