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目的在基因水平探讨人类巨细胞病毒(HCMV)感染导致脐血CFU-G损伤的机制,探讨人类脐血造血干细胞(HSC)向粒系祖细胞(CFU-G)增殖过程中hoxa9、hoxa10基因表达的情况。方法从2006年5月至2007年10月收集12例正常足月顺产新生儿断脐后的胎盘段脐血,采用造血干细胞体外培养技术及荧光定量逆转录聚合酶链反应(FQ-RT-PCR)方法,以HCMV-AD169和(或)全反式维甲酸(ATRA)持续干扰HSC,观察正常对照组、ATRA组、HCMV-AD169组、ATRA+HCMV组的造血干祖细胞经人粒细胞集落刺激因子(G-CSF)诱导后,在增殖分化过程中第3、7和12天检测CFU-Ghoxa9、hoxa10基因表达情况。结果各组hoxa9、hoxa10基因均在CFU-G增殖分化的第7天表达量最高(P<0.01),第12天表达量明显减弱(P<0.01),与正常对照组比较,CFU-Ghoxa9、hoxa10基因表达受ATRA(6×10-8mol/L)上调,而受HCMV下调(P<0.01),与HCMV组比较,ATRA可上调HCMV感染的CFU-Ghoxa9、hoxa10基因的表达。结论 CFU-G的增殖分化与hoxa9、hoxa10基因的表达相关。HCMV可能通过调控hoxa9、hoxa10基因表达异常引起造血功能异常,ATRA不仅能显著上调正常CFU-Ghoxa9、hoxa10基因的表达,而且能上调HCMV感染的CFU-Ghoxa9、hoxa10基因的表达。
Objective To investigate the mechanism of human cytomegalovirus (HCMV) infection in CFU-G induced by umbilical cord blood (HCMV) infection and to explore the expression of hoxa9 and hoxa10 during the proliferation of human umbilical cord blood hematopoietic stem cells (HSC) to granulocyte progenitor cells (CFU-G) Case. Methods From November 2006 to October 2007, 12 cases of normal full-term newborns with umbilical cord blood were collected from the placenta of umbilical cord. The hematopoietic stem cell culture in vitro and fluorescence quantitative reverse transcription polymerase chain reaction (FQ-RT-PCR) ), HCMV-AD169 and / or all-trans retinoic acid (ATRA) continued to interfere with HSC. The hematopoietic stem / progenitor cells in normal control, ATRA, HCMV-AD169 and ATRA + After induced by G-CSF, the expression of CFU-Ghoxa9 and hoxa10 gene were detected on the 3rd, 7th and 12th day after proliferation and differentiation. Results The expression of hoxa9 and hoxa10 gene in CFU-G group was the highest on the 7th day (P <0.01), and the expression of hoxa10 gene was significantly decreased on the 12th day (P <0.01). Compared with the normal control group, The expression of hoxa10 gene was up-regulated by ATRA (6 × 10-8 mol / L) and down-regulated by HCMV (P <0.01). Compared with HCMV group, ATRA up-regulated the expression of CFU-Ghoxa9 and hoxa10 in HCMV. Conclusion The proliferation and differentiation of CFU-G are correlated with the expression of hoxa9 and hoxa10. HCMV may cause hematopoietic dysfunction by regulating the expression of hoxa9 and hoxa10 gene abnormalities. ATRA can not only upregulate the expression of normal CFU-Ghoxa9 and hoxa10 gene, but also up-regulate the expression of CFU-Ghoxa9 and hoxa10 gene in HCMV infection.