Biology Department, Instituto de Biociências, Letras e Ciências Exatas, IBILCE-UNESP, Universidade Estadual Paulista "Júlio de Mesquita Filho,", Rua Cristóvão Colombo, 2265, São José do Rio Preto, São Paulo, 15054-000, Brazil.
Immunogenetics Laboratory, Molecular Biology Department, Faculdade de Medicina de São José do Rio Preto (FAMERP), Avenida Brigadeiro Faria Lima, 5416, Vila São Pedro, São José do Rio Preto, São Paulo, 15090-000, Brazil.
BMC Res Notes. 2020 Jul 9;13(1):328. doi: 10.1186/s13104-020-05166-3.
To determine the presence of the 7-bp deletion c.169+50delTAAACAG in intron 2 of Superoxide Dismutase-1 gene in keratoconic patients from the State of São Paulo, Brazil, which promotes splicing variations, resulting in non-functional Superoxide Dismutase-1 antioxidant proteins, which may damage the corneal structure.
A group of 35 keratoconic patients, from whom 35 peripheral blood samples and 58 samples of corneal fragments were evaluated, and a control group of 89 individuals, from whom 41 blood samples and 149 samples of corneal fragments were collected. After the amplification of DNA fragments by polymerase chain reaction, mutational screening analysis was performed by enzymatic digestion, followed by direct sequencing. The absence of the 7-bp c.169+50delTAAACAG mutation in intron 2 of Superoxide Dismutase-1 gene was detected in the analyzed subjects of the 2 groups, both in the cornea and peripheral blood samples. Then, according to our results, there is no involvement of c.169+50delTAAACAG deletion in the pathogenesis of keratoconus in this population, once it was not detected. But we emphasize that studies involving this deletion must be continued in an attempt to elucidate this issue.
在巴西圣保罗州的圆锥角膜患者中,确定超氧化物歧化酶-1 基因第 2 内含子中的 7-bp 缺失 c.169+50delTAAACAG 是否存在,该缺失会导致剪接变异,产生无功能的超氧化物歧化酶-1 抗氧化蛋白,从而破坏角膜结构。
我们评估了一组 35 名圆锥角膜患者,共采集了 35 份外周血样本和 58 份角膜碎片样本,以及一个对照组的 89 名个体,共采集了 41 份外周血样本和 149 份角膜碎片样本。通过聚合酶链反应扩增 DNA 片段后,进行酶消化的突变筛选分析,随后进行直接测序。在两组的分析对象中,无论是在角膜还是外周血样本中,都未检测到超氧化物歧化酶-1 基因第 2 内含子中 7-bp 的 c.169+50delTAAACAG 突变。因此,根据我们的结果,在该人群中,c.169+50delTAAACAG 缺失与圆锥角膜的发病机制无关,因为未检测到该缺失。但我们强调,必须继续进行涉及该缺失的研究,以阐明这个问题。