Buemi Michele, Allegra Alessandro, D'Anna Rosario, Coppolino Giuseppe, Crascì Eleonora, Giordano Domenico, Loddo Saverio, Cucinotta Maria, Musolino Caterina, Teti Diana
Department of Internal Medicine, Division of Hemathology, University of Messina, Messina, Italy.
Am J Obstet Gynecol. 2007 Jan;196(1):68.e1-6. doi: 10.1016/j.ajog.2006.08.032.
The aim of the present study was to analyze the concentrations of endothelial precursor cells (EPCs) during the 3 trimesters of normal pregnancy and to compare the EPC counts in women with normal pregnancy, gestational diabetes, and gestational hypertension.
The study was conducted on 21 pregnant women with single pregnancies (age range, 22 to 35 years). EPCs were quantified by flow cytometry. The subjects were divided into 3 groups, each consisting of 7 subjects: patients with gestational diabetes; patients with gestational hypertension; patients with normal pregnancy.
A progressive increase was found in the concentrations of EPCs during pregnancy in healthy women. In the third trimester of pregnancy, the number of CD34+ cells was significantly lower in patients with gestational diabetes than in hypertensive patients and controls; no significant differences were found between the levels of circulating CD34+ cells in hypertensive patients and those in controls. There were no significant differences between the diabetic and hypertensive patients for the percentage of cells expressing CD133 and VEGFR2, whereas in both groups the percentage of CD133+/VEGFR2+ elements was significantly higher than in the healthy control subjects.
Our findings confirm that EPCs isolated from the maternal circulation increase gradually throughout the gestational trimesters. These cells were derived from the endothelial cells lineage, as demonstrated by CD133+/VEGFR2+ cell assay. Moreover, the concentration of EPCs in pregnant women with gestational diabetes and hypertension differs from that in subjects with a normal pregnancy, CD34+ cells being reduced but CD133+/VEGFR2+ cell concentrations being increased. These results not only substantiate recent insights into the mechanisms regulating maternal vascular modifications during pregnancy but also throw light upon the activation of different patterns in the mobilization of endothelial progenitor cells during pathologic states in which endothelial disorders occur.
本研究旨在分析正常妊娠三个阶段内皮祖细胞（EPCs）的浓度，并比较正常妊娠、妊娠期糖尿病和妊娠期高血压女性的EPC计数。
对21名单胎妊娠孕妇（年龄范围22至35岁）进行了研究。通过流式细胞术对EPCs进行定量。受试者分为3组，每组7名受试者：妊娠期糖尿病患者；妊娠期高血压患者；正常妊娠患者。
健康女性孕期EPCs浓度呈逐渐上升趋势。在妊娠晚期，妊娠期糖尿病患者的CD34+细胞数量显著低于高血压患者和对照组；高血压患者与对照组循环CD34+细胞水平无显著差异。糖尿病患者和高血压患者之间表达CD133和VEGFR2的细胞百分比无显著差异，而两组中CD133+/VEGFR2+细胞的百分比均显著高于健康对照受试者。
我们的研究结果证实，从母体循环中分离出的EPCs在整个孕期逐渐增加。如CD133+/VEGFR2+细胞检测所示，这些细胞来源于内皮细胞谱系。此外，妊娠期糖尿病和高血压孕妇的EPCs浓度与正常妊娠受试者不同，CD34+细胞减少，但CD133+/VEGFR2+细胞浓度增加。这些结果不仅证实了近期对孕期母体血管变化调节机制的认识，也揭示了在内皮功能障碍的病理状态下内皮祖细胞动员的不同模式的激活情况。
