Over-Expression of Immune-Related lncRNAs in Inflammatory Demyelinating Polyradiculoneuropathies
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Over-Expression of Immune-Related lncRNAs in Inflammatory Demyelinating Polyradiculoneuropathies Saba Sadeghpour 1 & Soudeh Ghafouri-Fard 1 & Mehrdokht Mazdeh 2 & Fwad Nicknafs 1 & Naghme Nazer 3 & Arezou Sayad 1 & Mohammad Taheri 4 Received: 3 September 2020 / Accepted: 24 September 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Long non-coding RNAs (lncRNAs) have crucial roles in the pathogenesis of immune-related disorders. However, their role in the pathobiology of inflammatory demyelinating polyradiculoneuropathies remains unclear. In the current study, we measured peripheral expression of four lncRNAs, namely TUG1, FAS-AS1, NEAT1, and GAS5, in patients with acute/chronic inflammatory demyelinating polyradiculoneuropathies (AIDP/CIDP) compared with healthy subjects. Notably, all lncRNAs were overexpressed in patients compared with controls (P < 0.0001 for all lncRNAs). When assessing their expressions in AIDP and CIDP groups separately, TUG1 and NEAT1 were up-regulated in both patient groups compared with controls, yet FAS-AS1 and GAS5 were only up-regulated in CIDP cases. There were remarkable pairwise correlations between expression levels of these lncRNAs in all study groups. Based on the above-mentioned data, we suggest participation of these for lncRNAs in the pathogenesis of inflammatory demyelinating polyradiculoneuropathies. Moreover, FAS-AS1 and GAS5 lncRNAs have type-specific roles in this regard. Future functional studies are needed to elaborate the molecular mechanisms of the contribution of these transcripts in AIDP/CIDP. Keywords AIDP . CIDP . lncRNA . TUG1 . FAS-AS1 . NEAT1 . GAS5
Introduction Inflammatory demyelinating polyradiculoneuropathies (IDP) include a number of disorders that can be Saba Sadeghpour and Soudeh Ghafouri-Fard contributed equally to this work. Electronic supplementary material The online version of this article (https://doi.org/10.1007/s12031-020-01721-6) contains supplementary material, which is available to authorized users. * Arezou Sayad [email protected] * Mohammad Taheri [email protected] 1
Department of Medical Genetics, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
2
Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran
3
Department of Electrical Engineering, Sharif University of Technology, Tehran, Iran
4
Urogenital Stem Cell Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran
classified based on their acute or chronic clinical course to AIDP and CIDP disorders (Sangsefidi et al. 2020; Rezaei et al. 2020; Ali et al. 2020a, b). While CIDP is characterized as a chronic progressive, monophasic, or intermittent condition with a progressive stage of weakness that continues for 2 months (Van Den Bergh et al. 2010), AIDP has a period of less than 4 weeks of progression to clinical nadir (Dimachkie and Barohn 2013). AIDP is the most common type of Guillain– Barre syndrome (GBS) (Dimachkie and Barohn 2013). The immunological basis
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