端粒长度在新生儿造血干细胞和祖细胞辐射反应中的作用

IF 0.7 4区 医学 Q4 PATHOLOGY
Fetal and Pediatric Pathology Pub Date : 2024-07-01 Epub Date: 2024-08-06 DOI:10.1080/15513815.2024.2381752
Angshuman Biswas, Mandar Bhattacharya, Priyanka Ghosh, Subrata Kumar Dey
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引用次数: 0

摘要

目的:新生儿造血系统对电离辐射(IR)的反应存在广泛的个体差异,因此需要确定可靠的生物标志物来有效评估新生儿的辐射损伤:方法:通过评估166名健康新生儿的脐带血造血干细胞(HSC)的克隆分化,研究了其出生时端粒长度(TL)与辐射敏感性之间的关系。用 Southern 印迹法测定 TL 的末端限制性片段(TRF):结果:TL 与 0.75 Gy 时祖细胞集落形成细胞(CFC)总含量的存活部分相关(p p p p 结论:TL 与 0.75 Gy 时祖细胞集落形成细胞(CFC)总含量的存活部分相关:我们的研究结果表明,红外暴露后端粒较短的新生儿存在造血干细胞克隆存活风险。这些观察结果可能有助于将出生时的端粒长度作为评估与辐射相关的儿童造血挑战的一个因素。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Role of Telomere Length in Radiation Response of Hematopoietic Stem & Progenitor Cells in Newborns.

Objective: Wide inter-individual variations in ionizing radiation (IR) responses of neonatal hematopoietic system calls for identifying reliable biomarkers to effectively estimate radiation exposure damages in neonates.

Methods: Association between telomere length (TL) at birth and radiation sensitivity of cord blood hematopoietic stem cells (HSC) from 166 healthy newborns were investigated by assessing their clonogenic differentiation. TL was determined as terminal restriction fragment (TRF) by Southern blot method.

Results: TL correlated with surviving fractions of total progenitor colony forming cell (CFC) content at 0.75 Gy (p < 0.05), granulo-macrophagic lineage colony forming units (CFU-GM) at 0.75 Gy (p < 0.05) and erythroid burst forming unit (BFU-E) at 0.75 Gy (p < 0.05) & at 3 Gy (p < 0.05) of newborns.

Conclusion: Our results indicate risks for HSC clonogenic survival in neonates with shorter telomeres after IR exposure. These observations might aid in considering TL at birth as an assessment factor for radiation related hematopoietic challenges in children.

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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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