PedBE age and age acceleration in umbilical vein endothelial cells: an examination of infant birth outcomes.

IF 1.8 4区医学 Q3 PUBLIC, ENVIRONMENTAL & OCCUPATIONAL HEALTH

Journal of Developmental Origins of Health and Disease Pub Date : 2025-03-12 DOI:10.1017/S2040174424000333

Kristin M Voegtline, Radhika S Raghunathan, David W Sosnowski, Gang Peng, Cathrine Hoyo, Susan K Murphy, Raquel G Hernandez, Sara B Johnson

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引用次数: 0

Abstract

The current study examines the application of the Pediatric-Buccal-Epigenetic (PedBE) clock, designed for buccal epithelial cells, to endothelia. We evaluate the association of PedBE epigenetic age and age acceleration estimated from human umbilical vein endothelial cells (HUVECs) with length of gestation and birthweight in a racially and ethnically diverse sample (analytic sample n = 333). PedBE age was positively associated with gestational age at birth (r = 0.22, p < .001) and infant birth weight (r = 0.20, p < .001). Multivariate models revealed infants with higher birth weight (adjusted for gestational age) had greater PedBE epigenetic age acceleration (b = 0.0002, se = 0.0007, p = 0.002), though this effect was small; findings were unchanged excluding preterm infants born before 37 weeks' gestation. In conclusion, the PedBE clock may have application to endothelial cells and provide utility as an anchoring sampling point at birth to examine epigenetic aging in infancy.

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本研究探讨了将专为口腔上皮细胞设计的小儿-口腔-表观遗传学（Pediatric-Buccal-Epigenetic，PedBE）时钟应用于内皮细胞的问题。我们评估了从人脐静脉内皮细胞（HUVECs）估算出的 PedBE 表观遗传年龄和年龄加速度与不同种族和族裔样本（分析样本 n = 333）中妊娠期长度和出生体重的关系。PedBE 年龄与出生时的胎龄（r = 0.22，p < .001）和婴儿出生体重（r = 0.20，p < .001）呈正相关。多变量模型显示，出生体重越大的婴儿（根据胎龄调整），PedBE 表观遗传年龄加速度越大（b = 0.0002，se = 0.0007，p = 0.002），尽管这种影响很小；如果排除妊娠 37 周前出生的早产儿，研究结果不变。总之，PedBE 时钟可能适用于内皮细胞，并可作为出生时的锚定取样点来研究婴儿期的表观遗传衰老。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Journal of Developmental Origins of Health and Disease PUBLIC, ENVIRONMENTAL & OCCUPATIONAL HEALTH-

CiteScore

3.80

自引率

0.00%

发文量

145

审稿时长

6-12 weeks

期刊介绍： JDOHaD publishes leading research in the field of Developmental Origins of Health and Disease (DOHaD). The Journal focuses on the environment during early pre-natal and post-natal animal and human development, interactions between environmental and genetic factors, including environmental toxicants, and their influence on health and disease risk throughout the lifespan. JDOHaD publishes work on developmental programming, fetal and neonatal biology and physiology, early life nutrition, especially during the first 1,000 days of life, human ecology and evolution and Gene-Environment Interactions. JDOHaD also accepts manuscripts that address the social determinants or education of health and disease risk as they relate to the early life period, as well as the economic and health care costs of a poor start to life. Accordingly, JDOHaD is multi-disciplinary, with contributions from basic scientists working in the fields of physiology, biochemistry and nutrition, endocrinology and metabolism, developmental biology, molecular biology/ epigenetics, human biology/ anthropology, and evolutionary developmental biology. Moreover clinicians, nutritionists, epidemiologists, social scientists, economists, public health specialists and policy makers are very welcome to submit manuscripts. The journal includes original research articles, short communications and reviews, and has regular themed issues, with guest editors; it is also a platform for conference/workshop reports, and for opinion, comment and interaction.