State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat‑sen University, Guangzhou, Guangdong 510060, P.R. China.
Department of Toxicology, School of Public Health and Tropical Medicine, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Int J Mol Med. 2018 Feb;41(2):773-782. doi: 10.3892/ijmm.2017.3308. Epub 2017 Dec 5.
Familial exudative vitreoretinopathy (FEVR) is a rare hereditary retinal disorder characterized by the premature arrest of vascularization in the peripheral retina. The aim of the present study was to characterize the clinical presentations of a Chinese family affected by bilateral severe FEVR, and to identify the underlying genetic variations. One family that presented with bilateral FEVR was recruited for this study. Comprehensive ophthalmic examinations, including best‑corrected visual acuity, slit‑lamp examination, fundus photography, fundus fluorescein angiography imaging and electroretinogram were performed. Genomic DNA was extracted from leukocytes of the peripheral blood collected from the affected and unaffected family members, as well as 200 unrelated control subjects from the same population. Next‑generation sequencing of the candidate genes associated with ocular diseases was performed, and the identified mutations were validated by conventional polymerase chain reaction‑based sequencing. The functional effects of the mutations were analyzed by polymorphism phenotyping (PolyPhen) and sorting intolerant from tolerant (SIFT). One heterozygous ATP binding cassette subfamily A member 4 (ABCA4) c.5693G>A (p.R1898H) mutation in exon 40 and one heterozygous LDL receptor related protein 5 (LRP5) c.260T>G (p.I87S) mutation in exon 2 were identified in this family. To the best of our knowledge, the ABCA4 c.5693G>A (p.R1898H) mutation has not been reported in FEVR, and the LRP5 c.260T>G (p.I87S) mutation is a novel mutation. PolyPhen and SIFT predicted that the amino acid substitution R1898H in protein ABCA4 is benign, whereas the amino acid substitution I87S in protein LRP5 is damaging. A single nucleotide polymorphism c.266A>G (p.Q89R, rs41494349) was identified in exon 2 of LRP5. These findings expand the mutation spectrums of ABCA4 and LRP5, and will be valuable for genetic counseling and development of therapeutic interventions for patients with FEVR.
家族渗出性玻璃体视网膜病变(FEVR)是一种罕见的遗传性视网膜疾病,其特征是周边视网膜的血管化过早停止。本研究旨在描述一个受双侧严重 FEVR 影响的中国家庭的临床表现,并确定潜在的遗传变异。 一个有双侧 FEVR 表现的家庭被招募到这项研究中。 进行了全面的眼科检查,包括最佳矫正视力、裂隙灯检查、眼底照相、眼底荧光素血管造影成像和视网膜电图。 从外周血白细胞中提取受影响和未受影响的家庭成员以及来自同一人群的 200 名无关对照个体的基因组 DNA。 对与眼部疾病相关的候选基因进行下一代测序,并通过常规聚合酶链反应测序验证鉴定的突变。 通过多态性表型(PolyPhen)和耐受/不耐受排序(SIFT)分析突变的功能影响。 在该家庭中发现了一个杂合 ATP 结合盒亚家族 A 成员 4(ABCA4)c.5693G>A(p.R1898H)突变位于外显子 40 和一个杂合低密度脂蛋白受体相关蛋白 5(LRP5)c.260T>G(p.I87S)突变位于外显子 2。据我们所知,ABCA4 c.5693G>A(p.R1898H)突变在 FEVR 中尚未报道,而 LRP5 c.260T>G(p.I87S)突变是一种新的突变。 PolyPhen 和 SIFT 预测,蛋白质 ABCA4 中的氨基酸取代 R1898H 是良性的,而蛋白质 LRP5 中的氨基酸取代 I87S 是有害的。在外显子 2 中还发现了一个单核苷酸多态性 c.266A>G(p.Q89R,rs41494349)。这些发现扩展了 ABCA4 和 LRP5 的突变谱,对于 FEVR 患者的遗传咨询和治疗干预的发展将是有价值的。