β-arrestin1Regulate CD34+CD38-CD19+Cell Aging In Vivo

Objective: It has been reported that CD34+CD38+CD19+population，as well as CD34+CD38-CD19+population， can initiate andmaintain leukemia in NSG mice. At present, NSG mice and NOD/SCID,main immunodeficient mice, are applied to research the leukemia. The aimis that comparison the ability of propagation leukemia among the differentpopulations, and different mice.β-arrestin1regulates DNA damage through stress response, alongwith β2-adrenergic receptor. DNA damage is the main cause ofsenescence. We tried to observed that the impact of β-arrestin1onCD34+CD38-CD19+cell aging and investigated that whether β-arrestin1affected the CD34+CD38-CD19+cell aging via telomere, telomerase.Methods: Different population monocytes, isolated by MACS andidentified by FACS, injected into NSG mice via tail. The ability ofpropagation was compared among different population and different miceon WBC count in PB, blast cell in PB and BM, and HE stain. β-gal anddouble-population were used to monitor senescence. Southern blots, TRAPwere applied to detect the length of telomere, the activity of telomerase respectively. All statistics was performed on SPSS17.0.Results: The leukemia NSG mice, derived from CD34+CD38-CD19+mononuclear cell, had higher WBC count in PB, more blast cell in PB andBM and more serious infiltration in spleen, than the leukemia NSG micederived from other population. Shorter time for the peak of WBC count inPB, shorter survival time and more serious infiltration were observed inNSG mice than in NOD/SCID mice. Less positive rate of β-gal, shortertime for senescence, shorter the length of telomere and lower telomeraseactivity were attribute to Siβ-arrestin1. BIBR1532telomerase inhibitors(BIBR1532) could change the trend of telomere and telomerase, andincreased positive rate of β-gal and time for senescence were observed inNSG mice with BIBR1532.Conclusion: Although the ability of propagation was observed in allpopulations, the strongest propagation ability was observed inCD34+CD38-CD19+population. NSG mice than NOD/SCID mice wasmore suitable for leukemia research. β-arrestin1affected the senescence ofCD34+CD38-CD19+cell via telomere and telomerase.