Cross-Talk between Mitochondrial Dysfunction-Provoked Oxidative Stress and Aberrant Noncoding RNA Expression in the Pathogenesis and Pathophysiology of SLE
by
Chang-Youh Tsai 1,*,†
, Song-Chou Hsieh 2,†, Cheng-Shiun Lu 2,3, Tsai-Hung Wu 4, Hsien-Tzung Liao 1, Cheng-Han Wu 2,3, Ko-Jen Li 2, Yu-Min Kuo 2,3, Hui-Ting Lee 5, Chieh-Yu Shen 2,3 and Chia-Li Yu 2,*
Chang-Youh Tsai 1,*,†, Song-Chou Hsieh 2,†, Cheng-Shiun Lu 2,3, Tsai-Hung Wu 4, Hsien-Tzung Liao 1, Cheng-Han Wu 2,3, Ko-Jen Li 2, Yu-Min Kuo 2,3, Hui-Ting Lee 5, Chieh-Yu Shen 2,3 and Chia-Li Yu 2,*
1
Division of Allergy, Immunology & Rheumatology, Taipei Veterans General Hospital & National Yang-Ming University, #201 Sec.2, Shih-Pai Road, Taipei 11217, Taiwan
2
Department of Internal Medicine, National Taiwan University Hospital, #7 Chung-Shan South Road, Taipei 10002, Taiwan
3
Institute of Clinical Medicine, National Taiwan University College of Medicine, #7 Chung-Shan South Road, Taipei 10002, Taiwan
4
Division of Nephrology, Taipei Veterans General Hospital & National Yang-Ming University, #201 Sec. 2, Shih-Pai Road, Taipei 11217, Taiwan
5
Section of Allergy, Immunology & Rheumatology, Mackay Memorial Hospital, #92 Sec. 2, Chung-Shan North Road, Taipei 10449, Taiwan
*
Authors to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Int. J. Mol. Sci. 2019, 20(20), 5183; https://doi.org/10.3390/ijms20205183
Received: 10 September 2019 / Revised: 10 October 2019 / Accepted: 14 October 2019 / Published: 19 October 2019
(This article belongs to the Special Issue Crosstalk between MicroRNA and Oxidative Stress in Physiology and Pathology)
Systemic lupus erythematosus (SLE) is a prototype of systemic autoimmune disease involving almost every organ. Polygenic predisposition and complicated epigenetic regulations are the upstream factors to elicit its development. Mitochondrial dysfunction-provoked oxidative stress may also play a crucial role in it. Classical epigenetic regulations of gene expression may include DNA methylation/acetylation and histone modification. Recent investigations have revealed that intracellular and extracellular (exosomal) noncoding RNAs (ncRNAs), including microRNAs (miRs), and long noncoding RNAs (lncRNAs), are the key molecules for post-transcriptional regulation of messenger (m)RNA expression. Oxidative and nitrosative stresses originating from mitochondrial dysfunctions could become the pathological biosignatures for increased cell apoptosis/necrosis, nonhyperglycemic metabolic syndrome, multiple neoantigen formation, and immune dysregulation in patients with SLE. Recently, many authors noted that the cross-talk between oxidative stress and ncRNAs can trigger and perpetuate autoimmune reactions in patients with SLE. Intracellular interactions between miR and lncRNAs as well as extracellular exosomal ncRNA communication to and fro between remote cells/tissues via plasma or other body fluids also occur in the body. The urinary exosomal ncRNAs can now represent biosignatures for lupus nephritis. Herein, we’ll briefly review and discuss the cross-talk between excessive oxidative/nitrosative stress induced by mitochondrial dysfunction in tissues/cells and ncRNAs, as well as the prospect of antioxidant therapy in patients with SLE.
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Keywords:
noncoding RNA; microRNA; long noncoding RNA; mitochondrial dysfunction; oxidative stress; nitrosative stress. exosome; cross-talk; systemic lupus erythematosus
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited
MDPI and ACS Style
Tsai, C.-Y.; Hsieh, S.-C.; Lu, C.-S.; Wu, T.-H.; Liao, H.-T.; Wu, C.-H.; Li, K.-J.; Kuo, Y.-M.; Lee, H.-T.; Shen, C.-Y.; Yu, C.-L. Cross-Talk between Mitochondrial Dysfunction-Provoked Oxidative Stress and Aberrant Noncoding RNA Expression in the Pathogenesis and Pathophysiology of SLE. Int. J. Mol. Sci. 2019, 20, 5183.
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