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MESD 中的复合杂合移码突变导致致死性综合征,提示为成骨不全症 XX 型。

Compound Heterozygous Frameshift Mutations in MESD Cause a Lethal Syndrome Suggestive of Osteogenesis Imperfecta Type XX.

机构信息

Department of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Institute of Human Genetics, University Medical Center Göttingen, Göttingen, Germany.

出版信息

J Bone Miner Res. 2021 Jun;36(6):1077-1087. doi: 10.1002/jbmr.4277. Epub 2021 Mar 19.

Abstract

Multiple genes are known to be associated with osteogenesis imperfecta (OI), a phenotypically and genetically heterogenous bone disorder, marked predominantly by low bone mineral density and increased risk of fractures. Recently, mutations affecting MESD, which encodes for a chaperone required for trafficking of the low-density lipoprotein receptors LRP5 and LRP6 in the endoplasmic reticulum, were described to cause autosomal-recessive OI XX in homozygous children. In the present study, whole-exome sequencing of three stillbirths in one family was performed to evaluate the presence of a hereditary disorder. To further characterize the skeletal phenotype, fetal autopsy, bone histology, and quantitative backscattered electron imaging (qBEI) were performed, and the results were compared with those from an age-matched control with regular skeletal phenotype. In each of the affected individuals, compound heterozygous mutations in MESD exon 2 and exon 3 were detected. Based on the skeletal phenotype, which was characterized by multiple intrauterine fractures and severe skeletal deformity, OI XX was diagnosed in these individuals. Histological evaluation of MESD specimens revealed an impaired osseous development with an altered osteocyte morphology and reduced canalicular connectivity. Moreover, analysis of bone mineral density distribution by qBEI indicated an impaired and more heterogeneous matrix mineralization in individuals with MESD mutations than in controls. In contrast to the previously reported phenotypes of individuals with OI XX, the more severe phenotype in the present study is likely explained by a mutation in exon 2, located within the chaperone domain of MESD, that leads to a complete loss of function, which indicates the relevance of MESD in early skeletal development. © 2021 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR)..

摘要

已知多个基因与成骨不全症(OI)相关,OI 是一种表型和遗传异质性的骨骼疾病,主要表现为骨密度低和骨折风险增加。最近,描述了影响 MESD 的突变,该突变会影响内质网中 LDLR 受体 LRP5 和 LRP6 运输所需的伴侣,导致纯合子儿童常染色体隐性 OI XX。在本研究中,对一个家庭中的三个死胎进行了全外显子组测序,以评估遗传性疾病的存在。为了进一步描述骨骼表型,进行了胎儿尸检、骨组织学和定量背散射电子成像(qBEI),并将结果与具有常规骨骼表型的年龄匹配对照进行比较。在每个受影响的个体中,都检测到 MESD 外显子 2 和外显子 3 的复合杂合突变。基于骨骼表型,其特征是多次宫内骨折和严重骨骼畸形,这些个体被诊断为 OI XX。对 MESD 标本的组织学评估显示,骨发育受损,骨细胞形态改变,管腔连通性降低。此外,通过 qBEI 分析骨矿物质密度分布表明,与对照相比,MESD 突变个体的基质矿化受损且更不均匀。与先前报道的 OI XX 个体的表型不同,本研究中更严重的表型可能是由位于 MESD 伴侣结构域内的外显子 2 突变引起的,该突变导致完全丧失功能,表明 MESD 在早期骨骼发育中的相关性。© 2021 作者。由 Wiley 期刊公司代表美国骨骼矿物质研究协会(ASBMR)出版的《骨与矿物研究杂志》。

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