Gong Yi, Wu Yifan, Liu Yanli, Chen Sijie, Zhang Feiyu, Chen Feihong, Wang Chaowei, Li Shujin, Hu Minhan, Huang Ruitian, Xu Ke, Wang Xi, Yang Lei, Ning Yujie, Li Cheng, Zhou Rong, Guo Xiong
Department of Occupational and Environmental Health, School of Public Health, Xi'an Jiaotong University Health Science Center, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi'an, Shaanxi, China.
Department of Joint Surgery, Hong Hui Hospital, Xi'an Jiaotong University, Xi'an, China.
Front Cell Dev Biol. 2023 Feb 17;11:1083904. doi: 10.3389/fcell.2023.1083904. eCollection 2023.
Kashin-Beck disease (KBD) is a deformed osteochondral disease with a chronic progression that is restrictively distributed in eastern Siberia, North Korea, and some areas of China, and selenium deficiency has been identified as an important factor in the pathogenesis of this disease in recent years. The aim of this study is to investigate the selenoprotein transcriptome in chondrocytes and define the contribution of selenoprotein to KBD pathogenesis. Three cartilage samples were collected from the lateral tibial plateau of adult KBD patients and normal controls paired by age and sex for real-time quantitative polymerase chain reaction (RT-qPCR) to detect the mRNA expression of 25 selenoprotein genes in chondrocytes. Six other samples were collected from adult KBD patients and normal controls. In addition, immunohistochemistry was used on four adolescent KBD samples and seven normal controls (IHC) to determine the expression of proteins screened by RT-qPCR results that had different gene levels. Increased mRNA expression of GPX1 and GPX3 was observed in chondrocytes, and stronger positive staining was displayed in the cartilage from both adult and adolescent patients. The mRNA levels of DIO1, DIO2, and DIO3 were increased in KBD chondrocytes; however, the percentage of positive staining decreased in the KBD cartilage of adults. The selenoprotein transcriptome, mainly the glutathione peroxidase (GPX) and deiodinase (DIO) families were altered in KBD and might play a vital role in the pathogenesis of KBD.
大骨节病（KBD）是一种慢性进展性的畸形骨软骨病，主要分布于西伯利亚东部、朝鲜以及中国的一些地区，近年来研究发现硒缺乏是该病发病机制中的一个重要因素。本研究旨在探究软骨细胞中的硒蛋白转录组，并明确硒蛋白在大骨节病发病机制中的作用。从成年大骨节病患者和年龄及性别匹配的正常对照者的胫骨外侧平台采集三块软骨样本，采用实时定量聚合酶链反应（RT-qPCR）检测软骨细胞中25种硒蛋白基因的mRNA表达。另外从成年大骨节病患者和正常对照者中采集了六块其他样本。此外，对四份青少年大骨节病样本和七份正常对照样本进行免疫组化（IHC），以确定RT-qPCR结果中筛选出的不同基因水平的蛋白质的表达情况。在软骨细胞中观察到GPX1和GPX3的mRNA表达增加，在成年和青少年患者的软骨中均显示出更强的阳性染色。在大骨节病软骨细胞中DIO1、DIO2和DIO3的mRNA水平升高；然而，在成年大骨节病患者的软骨中阳性染色百分比降低。大骨节病中硒蛋白转录组发生改变，主要是谷胱甘肽过氧化物酶（GPX）和脱碘酶（DIO）家族，可能在大骨节病的发病机制中起重要作用。
