Methylation Status of IGF-Axis Genes in the Placenta of South Indian Neonates with Appropriate and Small for Gestational Age.

IF 0.7 4区医学 Q4 PATHOLOGY Fetal and Pediatric Pathology Pub Date : 2024-01-01 Epub Date: 2024-01-24 DOI:10.1080/15513815.2023.2280660

Nithya M N, Krishnappa J, Sheela S R, Venkateswarlu Raavi

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引用次数: 0

Abstract

Objective: Altered methylation patterns of insulin-like growth factor (IGF)-axis genes in small for gestational age (SGA) have been reported in different populations. In the present study, we analyzed the methylation status of IGF-axis genes in the placenta of appropriate for gestational age (AGA) and SGA neonates of South Indian women.

Methods: Placental samples were collected from AGA (n = 40) and SAG (n = 40) neonates. The methylation of IGF-axis genes promoter was analyzed using MS-PCR.

Results: IGF2, H19, IGF1, and IGFR1 genes promoter methylation was 2.5, 1.5, 5, and 7.5% lower in SGA compared to AGA, respectively. Co-methylation of IGF-axis genes promoter was 40% and 20% in AGA and SGA, respectively. IGF-axis gene promoter methylation significantly (p < 0.05) influenced the levels of IGFBP3 protein, birth weight, mitotic index, gestational weeks, and IGFR1 and IGFR2 gene expression.

Conclusion: IGF-axis genes methylation was lower in SGA than in AGA, and the methylation significantly influenced the IGF-axis components.

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南印度适龄和小胎龄新生儿胎盘中igf轴基因甲基化状态

目的:胰岛素样生长因子(IGF)轴基因甲基化模式改变在不同人群的小胎龄(SGA)已被报道。在本研究中，我们分析了南印度妇女适胎龄(AGA)和SGA新生儿胎盘中igf轴基因的甲基化状态。方法:采集AGA (n = 40)和SAG (n = 40)新生儿胎盘标本。采用MS-PCR分析igf轴基因启动子的甲基化。结果:IGF2、H19、IGF1和IGFR1基因启动子甲基化在SGA中分别比AGA低2.5%、1.5%、5%和7.5%。igf轴基因启动子共甲基化在AGA和SGA中分别为40%和20%。igf轴基因启动子甲基化显著(p IGFR1和IGFR2基因表达)。结论:igf -轴基因甲基化在SGA组低于AGA组，且甲基化显著影响igf -轴成分。

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来源期刊

Fetal and Pediatric Pathology 医学-病理学

CiteScore

3.00

自引率

0.00%

发文量

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.