PMID- 30907425
OWN - NLM
STAT- Publisher
LR  - 20240227
IS  - 1462-0332 (Electronic)
IS  - 1462-0324 (Linking)
DP  - 2019 Mar 25
TI  - Global analysis of protein expression in muscle tissues of 
      dermatomyositis/polymyosisits patients demonstrated an association between 
      dysferlin and human leucocyte antigen A.
LID - kez085 [pii]
LID - 10.1093/rheumatology/kez085 [doi]
AB  - OBJECTIVES: DM and PM are characterized by myofibre damage with inflammatory cell 
      infiltration due to the strong expressions of MHC class I HLA-A and monocyte 
      chemoattractant protein-1 (MCP-1). Dysferlin (DYSF) is a transmembrane 
      glycoprotein that anchors in the sarcolemma of myofibres. DYSF mutation is 
      closely associated with inherited myopathies. This study aimed to determine the 
      role of DYSF in the development of DM/PM. METHODS: Mass spectrometry was 
      performed in muscle tissues from DM/PM patients and controls. The DYSF levels in 
      muscle tissue, peripheral blood cells and serum were detected by Western 
      blotting, IF, flow cytometry or ELISA. Double IF and co-immunoprecipitation were 
      used to investigate the relationship between DYSF and HLA-A. RESULTS: Mass 
      spectrometry and bioinformatics analysis findings suggested the dysregulated 
      proteins in DM/PM patients participated in common biological processes and 
      pathways, such as the generation of precursor metabolites and energy. DYSF was 
      upregulated in the muscle tissue and serum of DM/PM patients. DYSF was mainly 
      expressed in myofibres and co-localized with HLA-A and MCP-1. DYSF and HLA-A 
      expressions were elevated in myocytes and endothelial cells after being 
      stimulated by patient serum and IFN-beta. However, no direct interactions were found 
      between DYSF and HLA-A by co-immunoprecipitation. CONCLUSION: Our study revealed 
      the dysregulated proteins involved in common and specific biological processes in 
      DM/PM patient samples. DYSF is upregulated and exhibits a potential role along 
      with that of HLA-A and MCP-1 in inflammatory cell infiltration and muscle damage 
      during the development of DM/PM.
CI  - (c) The Author(s) 2019. Published by Oxford University Press on behalf of the 
      British Society for Rheumatology. All rights reserved. For permissions, please 
      email: journals.permissions@oup.com.
FAU - Xiao, Yizhi
AU  - Xiao Y
AD  - Department of Rheumatology and Immunology, Xiangya Hospital, Central South 
      University, Changsha, China.
AD  - Institute of Rheumatology and Immunology, Central South University, Changsha, 
      China.
FAU - Zhu, Honglin
AU  - Zhu H
AD  - Department of Rheumatology and Immunology, Xiangya Hospital, Central South 
      University, Changsha, China.
AD  - Institute of Rheumatology and Immunology, Central South University, Changsha, 
      China.
FAU - Li, Liya
AU  - Li L
AD  - Department of Rheumatology and Immunology, Xiangya Hospital, Central South 
      University, Changsha, China.
AD  - Institute of Rheumatology and Immunology, Central South University, Changsha, 
      China.
FAU - Gao, Siming
AU  - Gao S
AD  - Department of Rheumatology and Immunology, Xiangya Hospital, Central South 
      University, Changsha, China.
AD  - Institute of Rheumatology and Immunology, Central South University, Changsha, 
      China.
FAU - Liu, Di
AU  - Liu D
AD  - Department of Rheumatology and Immunology, Xiangya Hospital, Central South 
      University, Changsha, China.
AD  - Institute of Rheumatology and Immunology, Central South University, Changsha, 
      China.
FAU - Dai, Bingying
AU  - Dai B
AD  - Department of Rheumatology and Immunology, Xiangya Hospital, Central South 
      University, Changsha, China.
AD  - Institute of Rheumatology and Immunology, Central South University, Changsha, 
      China.
FAU - Li, Qiuxiang
AU  - Li Q
AD  - Department of Neurology, Xiangya Hospital, Central South University, Changsha, 
      China.
FAU - Duan, Huiqian
AU  - Duan H
AD  - Department of Neurology, Xiangya Hospital, Central South University, Changsha, 
      China.
FAU - Yang, Huan
AU  - Yang H
AD  - Department of Neurology, Xiangya Hospital, Central South University, Changsha, 
      China.
FAU - Li, Quanzhen
AU  - Li Q
AD  - Department of Immunology, University of Texas Southwestern Medical Center, 
      Dallas, TX, USA.
FAU - Zhang, Huali
AU  - Zhang H
AD  - Department of Pathophysiology, Xiangya School of Medicine, Central South 
      University, Changsha, China.
FAU - Luo, Hui
AU  - Luo H
AD  - Department of Rheumatology and Immunology, Xiangya Hospital, Central South 
      University, Changsha, China.
AD  - Institute of Rheumatology and Immunology, Central South University, Changsha, 
      China.
FAU - Zuo, Xiaoxia
AU  - Zuo X
AD  - Department of Rheumatology and Immunology, Xiangya Hospital, Central South 
      University, Changsha, China.
AD  - Institute of Rheumatology and Immunology, Central South University, Changsha, 
      China.
LA  - eng
PT  - Journal Article
DEP - 20190325
PL  - England
TA  - Rheumatology (Oxford)
JT  - Rheumatology (Oxford, England)
JID - 100883501
OTO - NOTNLM
OT  - DYSF
OT  - HLA-A
OT  - dermatomyositis
OT  - polymyositis
OT  - protein profiles
EDAT- 2019/03/26 06:00
MHDA- 2019/03/26 06:00
CRDT- 2019/03/26 06:00
PHST- 2018/11/08 00:00 [received]
PHST- 2019/02/04 00:00 [revised]
PHST- 2019/03/26 06:00 [entrez]
PHST- 2019/03/26 06:00 [pubmed]
PHST- 2019/03/26 06:00 [medline]
AID - 5419312 [pii]
AID - 10.1093/rheumatology/kez085 [doi]
PST - aheadofprint
SO  - Rheumatology (Oxford). 2019 Mar 25:kez085. doi: 10.1093/rheumatology/kez085.