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IL17RC Affects the Predisposition to Thoracic Ossification of the Posterior

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IL17RC Affects the Predisposition to Thoracic Ossification of the Posterior Wang et al. Journal of Orthopaedic Surgery and Research (2019) 14:210 https://doi.org/10.1186/s13018-019-1253-3 RESEARCH ARTICLE Open Access IL17RC affects the predisposition to thoracic ossification of the posterior longitudinal ligament Peng Wang1,2, Xiaoguang Liu3, Xiao Liu3, Chao Kong1,2, Ze Teng4, Yunlong Ma3, Lei Yong3, Chen Liang3, Guanping He3 and Shibao Lu1,2* Abstract Background: Thoracic ossification of the posterior longitudinal ligament (T-OPLL) can cause thoracic spinal stenosis, which results in intractable myelopathy and radiculopathy. The etiology of T-OPLL is unknown and the condition is difficult to treat surgically. Whole-genome sequencing identified a genetic variant at rs199772854 of the interleukin 17 receptor C (IL17RC) gene as a potentially pathogenic locus associated with T-OPLL. We aimed to determine whether the rs199772854A site mutation causes abnormal expression of the IL17RC in Han Chinese patients with T-OPLL and predict the possible pathogenic mechanisms of T-OPLL. Analyses were performed to determine whether IL17RC is involved in the pathogenicity of T-OPLL. Methods: Peripheral blood and OPLL tissue were collected from a total of 72 patients with T-OPLL disease (36 patients carrying the rs199772854A site mutation in IL17RC and 36 wild-type patients). The expression of IL17RC was analyzed by enzyme-linked immunosorbent assay, reverse transcription-quantitative polymerase chain reaction, immunohistochemistry, and Western blotting. Results: rs199772854A mutation resulted in markedly increased IL17RC gene expression levels in peripheral blood samples and the OPLL tissue obtained following clinical surgery (P <0.05). Conclusions: The results suggest that the rs199772854A site mutation of IL17RC can significantly increase the expression of IL17RC. The IL17RC gene rs199772854A site polymorphism is a potential pathogenic mutation in T-OPLL disease, which may be associated with the occurrence of T-OPLL. Keywords: IL17RC, Thoracic ossification of the posterior longitudinal ligament Background cervical OPLL (C-OPLL). T-OPLL has a marked ethnic Thoracic ossification of the posterior longitudinal liga- predilection, as this disease occurs more frequently in ment (T-OPLL) is characterized by pathological hetero- Japanese and Chinese individuals. The prevalence of T- topic ossification of this region. T-OPLL is one of the OPLL in individuals of Japanese ethnicity is 1.6–1.9%, common factors that cause thoracic spinal stenosis, and the mean age of onset is > 40 years old [1, 2]. which results in intractable myelopathy and radiculopa- Conservative treatments are typically ineffective for thy. Early diagnosis of the disease is difficult, as the ma- T-OPLL, with surgery as the only effective treatment. jority of patients develop symptoms only when the However, due to the unique anatomy and patho- ossified ligament severely compresses the spinal cord. physiological factors associated with for T-OPLL, T-OPLL causes a much higher rate of disability than postoperative cerebrospinal fluid leakage, paraplegia, infection, and other complications are common, oc- * Correspondence: [email protected] curring in 9.6–40.8% of patients that receive surgical 1 Department of Orthopedics, Xuanwu Hospital of Capital Medical University, treatment [3–5], and the pathogenesis of T-OPLL re- 45 Changchun Street, Xicheng, Beijing 100053, People’s Republic of China 2National Clinical Research Center for Geriatric Diseases, Beijing 100053, mains unclear. Most studies suggest that C-OPLL is a People’s Republic of China ‘genetic’ disease [6–16], the thoracic spine experiences Full list of author information is available at the end of the article © The Author(s). 2019 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. Wang et al. Journal of Orthopaedic Surgery and Research (2019) 14:210 Page 2 of 8 less local biological stress than the cervical spine; thus, we speculate that genetic factors may contribute to the development of T-OPLL. Our previous whole- genome sequencing and candidate gene-association studies demonstrated that the presence of the rs199 772854A single-nucleotide polymorphism (SNP) in the interleukin 17 receptor C (IL17RC) gene is poten- tially associated with T-OPLL susceptibility [17, 18]. Therefore, we hypothesize that IL17RC might be in- volved in the formation of OPLL of the thoracic spine. The IL17RC gene is located at chromosome region 3p25.3-3p24.1 and encodes a type I transmembrane protein [19]. IL17RC is a proinflammatory receptor with a crucial role in the development of osteoblasts and accelerates osteoblast differentiation [20]. As OPLL promotes bone formation in ligament tissue, OPLL is associated with increased bone mineral density. The present study aimed to determine whether the rs199772854A site mutation causes abnormal expression of the IL17RC gene in patients with T-OPLL among a Han Chinese population and to determine whether Fig. 1 OPLL specimens of the thoracic spine. T-OPLL specimens IL17RC is involved in the pathogenicity of T-OPLL. removed by circumferential decompression surgery in patients with T-OPLL. OPLL ossified posterior longitudinal ligament, T-OPLL thoracic OPLL Materials and methods Disease criteria and patients duplicate. The optical density of each well was determined This retrospective study protocol was approved by the using a microplate reader at 450 nm. No interference and ethical committee for human subjects of the Peking Uni- no cross reactivity were expected based on the manufac- versity Third Hospital (Beijing, China). Informed consent turer’sinstructions. was provided by all participating individuals. Unrelated northern Chinese Han patients with T-OPLL carrying the rs199772854A site mutation in IL17RC and unrelated Reverse transcription-quantitative polymerase chain northern Chinese Han patients with T-OPLL carrying the reaction wild-type rs199772854C site were enrolled in this study Total RNA was purified from blood using the SK1321 between May 2014 and July 2018. Diagnosis of T-OPLL RNA Blood Mini Kit (Sangon Biotech Co., Ltd., Shanghai, was performed by orthopedic spine specialists based on China). A one-column DNase digest (Sangon Biotech Co., clinical symptoms and computed tomography (CT) of the Ltd.) was performed before the clean-up step to eliminate thoracic spine. The appearance of T-OPLL observed in residual genomic DNA. cDNA was synthesized from total CT was classified as segmental, continuous, mixed, or RNA (2 μg)usingaRevertAidPremiumReverseTran- local disease type [21]. Neurological status was evaluated scriptase kit (Thermo Fisher Scientific, Inc., Waltham, MA, by the Japanese Orthopedic Association (JOA) score for USA). Relative qPCR was applied to quantify the mRNAs thoracic myelopathy (maximum 11 points). The posterior levels of IL17RC using SYBR Green Real-Time PCR master longitudinal ligament specimens of the thoracic spine in mix on the LightCycler480 Real-Time System (Roche Diag- patients with T-OPLL were collected during circumferen- nostics, Basel, Switzerland). All experiments were per- tial decompression surgery (Fig. 1). formed in triplicate and normalized to glyceraldehyde-3- phosphate dehydrogenase (GAPDH). Details of the primer Plasma IL17RC enzyme-linked immunosorbent assay sequences are listed in Table 1. Plasma collection and storage were performed using standard methods. Plasma IL17RC levels were quantified Hematoxylin-eosin staining and immunohistochemistry using commercially available enzyme-linked immunosorb- analysis ent assay (ELISA) kits (Trust Specialty Zeal, Inc., San Serial 5-mm-thick sections were prepared from Francisco, CA, USA). All samples were assayed according paraffin-embedded thoracic spine specimens for stain- to the manufacturer’s instructions and were run in ing. Hematoxylin-eosin staining was performed in an Wang et al. Journal of Orthopaedic Surgery and Research (2019) 14:210 Page 3 of 8 Table 1 Primer sequences used for quantitative polymerase Protein levels were quantified by densitometry analysis chain reaction using Image-Pro Plus 6.0 software (Media Cybernetics, Gene Primer sequence Inc., Rockville, MD, USA). Beta-actin was used as the IL17RC Forward 5′-TATGGGACGATGACTTGGGA-3′ endogenous control. Reverse 5′-TGAGAAGGAGGATGAGGGAAA-3′ GAPDH Forward 5′-TGGGTGTGAACCATGAGAAGT-3′ Statistical analysis ′ ′ Reverse 5 -GAGTCCTTCCACGATACCAA-3 All statistical analyses were performed using SPSS v17.0 software (SPSS, Inc., Chicago, IL, USA). Descriptive data autostainer machine (Leica Microsystems GmbH, for continuous variables are presented as the mean ± Mannheim, Germany) using standard procedures. Sec- standard deviations. Student’s t test was used to compare tions for immunohistochemical (IHC) staining were age, gender, and JOA score differences between T-OPLL deparaffinized using xylene and dehydrated in serially patients with different IL17RC gene variants. The differ- graded ethanol solutions. The sections were washed ences in T-OPLL subtypes between patients with or in distilled water,
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