Functional network analysis reveals biological roles of lncRNAs and mRNAs in MOG35-55 specific CD4+T helper cells

Zhaoying Li; Pixia Gong; Wen Wang; Siying Qu; Xi Wang; Zhongze He; Guangyou Wang; Qingfei Kong; Lili Mu; Jinghua Wang; Shaohong Fang; Wei Zhao; Bo Sun; Hulun Li

doi:10.1016/j.ygeno.2018.01.012

Functional network analysis reveals biological roles of lncRNAs and mRNAs in MOG_35-55 specific CD4⁺T helper cells

Genomics. 2018 Nov;110(6):337-346. doi: 10.1016/j.ygeno.2018.01.012. Epub 2018 Jan 31.

Authors

Zhaoying Li¹, Pixia Gong¹, Wen Wang², Siying Qu¹, Xi Wang¹, Zhongze He¹, Guangyou Wang¹, Qingfei Kong¹, Lili Mu¹, Jinghua Wang¹, Shaohong Fang³, Wei Zhao¹, Bo Sun⁴, Hulun Li⁵

Affiliations

¹ Department of Neurobiology, Harbin Medical University, Heilongjiang Provincial Key Laboratory of Neurobiology, Harbin, Heilongjiang 150081, China.
² Peking Union Medical College,Tsinghua University, Beijing 100000, China.
³ The Key Laboratory of Myocardial Ischemia, Chinese Ministry of Education, Harbin, Heilongjiang Province 150086, China; Department of Cardiology, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, China.
⁴ Department of Neurobiology, Harbin Medical University, Heilongjiang Provincial Key Laboratory of Neurobiology, Harbin, Heilongjiang 150081, China. Electronic address: [email protected].
⁵ Department of Neurobiology, Harbin Medical University, Heilongjiang Provincial Key Laboratory of Neurobiology, Harbin, Heilongjiang 150081, China; The Key Laboratory of Myocardial Ischemia, Chinese Ministry of Education, Harbin, Heilongjiang Province 150086, China. Electronic address: [email protected].

PMID: 29366861
DOI: 10.1016/j.ygeno.2018.01.012

Abstract

Long non-coding RNAs have the potential to regulate immune responses. Their impact on multiple sclerosis has remained elusive. For illustrating their roles in experimental autoimmune encephalomyelitis (EAE) pathogenesis, we investigated the differential expression of lncRNAs and mRNAs in CD4⁺Th cells obtained from myelin oligodendrocytic glycoprotein_35-55(MOG_35-55)-induced EAE and complete Freund's adjuvant (CFA) controls. We observed differential expression of 1112 lncRNAs and 519 mRNAs in CD4⁺Th cells. The functional network showed lncRNAs had the capacity to modulate EAE pathogenesis via regulating many known EAE regulators such as Ptpn6. Predicting the function of lncRNAs demonstrated that dysregulated lncRNAs were closely associated with the development of EAE. These dysregulated lncRNAs may have function in EAE and they could be novel biomarkers and therapeutic targets of EAE. However, the precise mechanisms and biological functions of these specific lncRNAs in EAE pathogenesis require further study.

Keywords: CD4(+)Th cell; Experimental autoimmune encephalomyelitis; Gene expression; Long non-coding RNA; mRNA.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Animals
Encephalomyelitis, Autoimmune, Experimental / genetics
Encephalomyelitis, Autoimmune, Experimental / metabolism*
Female
Gene Expression Profiling
Gene Expression Regulation*
Mice
Myelin-Oligodendrocyte Glycoprotein / pharmacology
Myelin-Oligodendrocyte Glycoprotein / toxicity
Protein Tyrosine Phosphatase, Non-Receptor Type 6 / genetics
Protein Tyrosine Phosphatase, Non-Receptor Type 6 / metabolism
RNA, Long Noncoding / genetics*
RNA, Messenger / genetics*
T-Lymphocytes, Helper-Inducer / drug effects
T-Lymphocytes, Helper-Inducer / metabolism*

Substances

Myelin-Oligodendrocyte Glycoprotein
RNA, Long Noncoding
RNA, Messenger
Protein Tyrosine Phosphatase, Non-Receptor Type 6
Ptpn6 protein, mouse