Linyi Peng1, Weizhi Ma1, Fan Yi1, Yun-Jiao Yang1, Wei Lin1, Hua Chen1, Xuan Zhang1, Li-He Zhang1, Fengchun Zhang1, Quan Du2. 1. From the Department of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital; Chinese Academy of Medical Sciences and Peking Union Medical College; State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University; Key Laboratory of Rheumatology and Clinical Immunology, Ministry of Education, Beijing, China.L. Peng, PhD, Department of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Key Laboratory of Rheumatology and Clinical Immunology, Ministry of Education; W. Ma, BS; F. Yi, PhD, State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University; Y-J. Yang, PhD; W. Lin, BS; H. Chen, PhD; X. Zhang, PhD, Department of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Key Laboratory of Rheumatology and Clinical Immunology, Ministry of Education; L-H. Zhang, PhD, State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University; F. Zhang, PhD, Department of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Key Laboratory of Rheumatology and Clinical Immunology, Ministry of Education; Q. Du, PhD, State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University. 2. From the Department of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital; Chinese Academy of Medical Sciences and Peking Union Medical College; State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University; Key Laboratory of Rheumatology and Clinical Immunology, Ministry of Education, Beijing, China.L. Peng, PhD, Department of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Key Laboratory of Rheumatology and Clinical Immunology, Ministry of Education; W. Ma, BS; F. Yi, PhD, State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University; Y-J. Yang, PhD; W. Lin, BS; H. Chen, PhD; X. Zhang, PhD, Department of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Key Laboratory of Rheumatology and Clinical Immunology, Ministry of Education; L-H. Zhang, PhD, State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University; F. Zhang, PhD, Department of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Key Laboratory of Rheumatology and Clinical Immunology, Ministry of Education; Q. Du, PhD, State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University. quan.du@pku.edu.cn.
Abstract
OBJECTIVE: Characterized by chronic inflammation, dysfunction of exocrine glands, and systemic autoimmunity, primary Sjögren syndrome (pSS) is a common autoimmune disease in elderly women. Our study was performed to explore the potential involvement of microRNA (miRNA) in Chinese patients with pSS. METHODS: Using microarrays, miRNA expression in peripheral blood mononuclear cells (PBMC) was profiled in 4 female patients with pSS and 3 healthy participants, followed by a large-scale study of 33 patients and 10 healthy individuals. Compared to the healthy participants, 202 miRNA were upregulated and 180 were downregulated in the patients with pSS. To confirm this finding, a set of regulated miRNA was further examined in a large patient group, using quantitative reverse transcriptase-PCR assays. RESULTS: MiR-181a was the miRNA that most profoundly differed between patients with pSS and healthy individuals; however, similar miRNA-181a expression profiles were found in groups with different disease phenotypes. Together, these observations suggested that an elevated miRNA-181a level is a general phenomenon in Chinese patients with pSS. CONCLUSION: In addition to the elevated miR-181a levels, our study led to the speculation that elevated miR-181a levels in the PBMC of these patients compromise the maturation of B cells, enabling them to recognize and attack autoantigens and resulting in disease phenotypes. In addition to the regulation of human miRNA, many virus-derived miRNA were unexpectedly upregulated in the patients with pSS, suggesting that viral infection of PBMC plays a role in this disease.
OBJECTIVE: Characterized by chronic inflammation, dysfunction of exocrine glands, and systemic autoimmunity, primary Sjögren syndrome (pSS) is a common autoimmune disease in elderly women. Our study was performed to explore the potential involvement of microRNA (miRNA) in Chinese patients with pSS. METHODS: Using microarrays, miRNA expression in peripheral blood mononuclear cells (PBMC) was profiled in 4 female patients with pSS and 3 healthy participants, followed by a large-scale study of 33 patients and 10 healthy individuals. Compared to the healthy participants, 202 miRNA were upregulated and 180 were downregulated in the patients with pSS. To confirm this finding, a set of regulated miRNA was further examined in a large patient group, using quantitative reverse transcriptase-PCR assays. RESULTS:MiR-181a was the miRNA that most profoundly differed between patients with pSS and healthy individuals; however, similar miRNA-181a expression profiles were found in groups with different disease phenotypes. Together, these observations suggested that an elevated miRNA-181a level is a general phenomenon in Chinese patients with pSS. CONCLUSION: In addition to the elevated miR-181a levels, our study led to the speculation that elevated miR-181a levels in the PBMC of these patients compromise the maturation of B cells, enabling them to recognize and attack autoantigens and resulting in disease phenotypes. In addition to the regulation of human miRNA, many virus-derived miRNA were unexpectedly upregulated in the patients with pSS, suggesting that viral infection of PBMC plays a role in this disease.
Entities:
Keywords:
MICRORNA-181A; SJÖGREN SYNDROME; T CELL MATURATION
Authors: Adrienne E G Williams; Kevin Choi; Annie L Chan; Yun Jong Lee; Westley H Reeves; Michael R Bubb; Carol M Stewart; Seunghee Cha Journal: Arthritis Res Ther Date: 2016-05-03 Impact factor: 5.156