Al-Mufti R, Hambley H, Farzaneh F, Nicolaides K H
Harris Birthright Research Centre For Fetal Medicine, Denmark Hill, London, England.
Haematologica. 2000 Jul;85(7):690-3.
During fetal development a change in erythropoiesis from hepatic to medullary site occurs. In chromosomally abnormal fetuses this change is delayed. Hemoglobin production also undergoes developmental switches from embryonic to fetal hemoglobins in the first trimester of pregnancy. The aim of study was to determine the proportion of embryonic and fetal hemoglobins in fetal erythroblasts of chromosomally normal and abnormal fetuses at 10-40 weeks of gestation.
Fetal blood was obtained from 93 chromosomally normal and 19 abnormal fetuses at 10-40 weeks of gestation. Fetal erythroblasts were isolated by triple density gradient centrifugation and magnetic cell sorting with CD71 antibody. Fluorescent antibodies were used to immuno-stain for zeta (zeta), epsilon (epsilon) and gamma (gamma) hemoglobin chains.
The percentages of the positively stained cells were calculated. In chromosomally normal fetuses the percentage of erythroblasts expressing the zeta chain was 25% at 10 weeks but this decreased exponentially with gestation to less than 1% by 17 weeks. Similarly, the percentage of cells expressing the epsilon chain decreased from 97% at 10 weeks to less than 1% by 25 weeks. In contrast, expression of the gamma chain increased from about 30% at 10 weeks to 90% by 16 weeks and decreased thereafter to 60% at 40 weeks. In the abnormal fetuses, the percentage of erythroblasts expressing the zeta chain and the epsilon chain decreased to less than 1% by 23 and 28 weeks respectively, while maximum expression of the gamma chain was at about 22 weeks.
In the chromosomally abnormal group the pattern of change in the expression of the various hemoglobin chains during gestation was similar to that in the normal fetuses but was delayed by three to six weeks. These findings suggest that in fetuses with chromosomal abnormalities there is a developmental delay in the switch from embryonic to fetal hemoglobin chains.
在胎儿发育过程中，红细胞生成部位从肝脏转变为骨髓。在染色体异常的胎儿中，这种转变会延迟。血红蛋白的产生在妊娠早期也会经历从胚胎血红蛋白到胎儿血红蛋白的发育转换。本研究的目的是确定妊娠10 - 40周时染色体正常和异常胎儿的胎儿成红细胞中胚胎血红蛋白和胎儿血红蛋白的比例。
从93例染色体正常和19例染色体异常的妊娠10 - 40周胎儿获取胎儿血液。通过三重密度梯度离心和用CD71抗体进行磁性细胞分选分离胎儿成红细胞。使用荧光抗体对ζ（zeta）、ε（epsilon）和γ（gamma）血红蛋白链进行免疫染色。
计算阳性染色细胞的百分比。在染色体正常的胎儿中，表达ζ链的成红细胞百分比在10周时为25%，但随着孕周呈指数下降，到17周时降至1%以下。同样，表达ε链的细胞百分比从10周时的97%降至25周时的1%以下。相比之下，γ链的表达从10周时的约30%增加到16周时的90%，此后下降，到40周时降至60%。在异常胎儿中，表达ζ链和ε链的成红细胞百分比分别在23周和28周时降至1%以下，而γ链的最大表达约在22周。
在染色体异常组中，妊娠期间各种血红蛋白链表达的变化模式与正常胎儿相似，但延迟了三到六周。这些发现表明，染色体异常的胎儿在从胚胎血红蛋白链向胎儿血红蛋白链的转换中存在发育延迟。
