GADD45B在IgA肾病患儿肾组织中的表达及其与肾小球系膜肥大的关系。

IF 0.7 4区 医学 Q4 PATHOLOGY
Fetal and Pediatric Pathology Pub Date : 2023-10-01 Epub Date: 2023-08-03 DOI:10.1080/15513815.2023.2239904
Chong Li, Ailing Wei, Yuanhan Qin
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引用次数: 0

摘要

背景:我们将IgA肾病(IgAN)肾组织中生长停滞和DNA损伤诱导蛋白β(GADD45B)的表达与临床特征和系膜高细胞性相关。材料和方法:根据Oxford分类将IgAN儿童的活检分为M0组和M1组,并选择患有微小变化疾病(MCD)的活检作为对照。在PAS染色的组织上评估系膜细胞增殖区域,并通过免疫组织化学染色(IHC)评估肾组织中GADD45B的相对水平。结果:与MCD组相比,M0和M1组的GADD45B水平显著升高(p 结论:GADD45B的高表达可能在肾小球系膜高细胞性中起调节作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Expression of GADD45B in Renal Tissue of Children with IgA Nephropathy and Correlation with Mesangial Hypercellularity.

Background: We correlated the expression of growth arrest and DNA damage-inducible protein beta (GADD45B) in renal tissue with IgA nephropathy (IgAN) with clinical characteristics and mesangial hypercellularity. Materials and methods: Biopsies from IgAN children were divided into M0 and M1 groups based on the Oxford classification, and biopsies with minimal change disease (MCD) were selected as controls. The mesangial cell proliferation area was evaluated on PAS-stained tissues, and the relative level of GADD45B in renal tissue was assessed by immunohistochemical staining (IHC). Results: Compared with the MCD group, levels of GADD45B in the M0 and M1 groups were significantly higher (p < 0.05). Levels of GADD45B positively correlated with mesangial cell proliferation, proteinuria, and total cholesterol, negatively correlated with Alb levels. Conclusions: It is suggested that high expression of GADD45B may play a regulatory role in mesangial hypercellularity.

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来源期刊
CiteScore
3.00
自引率
0.00%
发文量
68
审稿时长
6-12 weeks
期刊介绍: Fetal and Pediatric Pathology is an established bimonthly international journal that publishes data on diseases of the developing embryo, newborns, children, and adolescents. The journal publishes original and review articles and reportable case reports. The expanded scope of the journal encompasses molecular basis of genetic disorders; molecular basis of diseases that lead to implantation failures; molecular basis of abnormal placentation; placentology and molecular basis of habitual abortion; intrauterine development and molecular basis of embryonic death; pathogenisis and etiologic factors involved in sudden infant death syndrome; the underlying molecular basis, and pathogenesis of diseases that lead to morbidity and mortality in newborns; prenatal, perinatal, and pediatric diseases and molecular basis of diseases of childhood including solid tumors and tumors of the hematopoietic system; and experimental and molecular pathology.
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