ABSTRACT
BACKGROUND: There are small amount of hematopoietic stem cells, which are easy to divide in vitro and show the difficulty in applying to transplantation.OBJECTIVE: This paper has focused on the role and means of the Wnt, Notch, Bmi_1, Shh, HOXB4 signaling molecule in the maintenance of hematopoietic stem cell self-renewal and regulation. METHODS: With the key words of "HSC, Wnt, Notch, Bmi_1, Shh, HOXB4" for the search, we searched PubMed database (2002-01/2008-12) in English. Literatures closely related to the hematopoietic stem cell self-renewal related signaling molecules were included. Repetitive research and Meta analysis were excluded.RESULTS AND CONCLUSION: The computer initially retrieved 216 documents, of which 30 documents for research. Hematopoietic stem cells are self-renewing, have strong differentiation and growth and regeneration capacities, can produce various types of blood cells ancestor cells, are widely used to treat blood diseases, but the hematopoietic stem cell differentiation in vitro demonstrated that the difficulties used in transplantation. How to make hematopoietic stem cells in vitro amplification and processing, while maintaining hematopoietic stem cell self-renewal characteristics is of a key issue. In recent years, different signaling pathways to enhance the ability of hematopoietic stem cell self-renewal signaling molecule have been a research hotspot. The article focused on the role and means of the Wnt, Notch, Bmi_1, Shh, HOXB4 in the maintenance of hematopoietic stem cell self-renewal and regulation and found that both the above-mentioned five signaling molecules can enhance hematopoietic stem cell self-renewal function. There are also a number of factors playing an important role in the maintenance of hematopoietic stem cell self-renewal process, such as endogenous factors, a series of transcription factors Oct-4, Ehox, Nanog, SCL, Runx1 and so on, to explore how their regulatory networks formed by the interaction control self-renewal of hematopoietic stem cells will become a key point in the research of self-renewal of hematopoietic stem cells.
ABSTRACT
BACKGROUND:Some studies show that basic fibroblast growth factor(bFGF)strongly expresses dudng the process of embryonic stem cells differentiation into hematopoietic stem cell.yolk sac blooding.and fetal liver hematopoiesis.OBJECTIVE:To study the regulation of bFGF on the blast-colony-forming cell(BL-CFC)by adding bFGF in the medium of embryoid body generation.METHODS:The third to fifth generations of the pdmaw mouse embryonic fibroblasts were recovered,and then incubated with the DMEM medium containing mitomvcin C for 2.5 hours in order to lose the proliferative capacity.Then cells were suspended into single cell by trypsinization and inoculated in the gelatin-coated bottle at the density of 10×104/cm2.After culturing for 24 hours,mouse embryonic stem cells(mESC)of D3 were recovered and placed on the feeder layer cells.According to the composition of medium in embryoid body generation.mESCs were divided into two groups:group A:standard medium+VEGF+SCF;group B:standard medium+VEGF+SCF+bFGF.Each group was cultured for 3 days and 6 days respectively,and the cloning number of BL-CFC was quantified,as well as Flk-1+ expression was observed by immunofluorescence staining.Positive number and average absorbance were analyzed using IMAGE-PRO PLUS imaging analysis system.RESULTS AND CONCLUSION:Adding bFGF in the course of embryoid body growth could significantly increase the number of BL-CFC(P＜0.01).and the positive results of Flk-1 and the average absorbance were also increased significantly(P＜0.01).bFGF effectively promoted embryoid body amplification and proliferation of BL-CFC.
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AIM: To observe the changes of interleukin-6(IL-6), IL-8 and tumor necrosis factor-?(TNF-?) in serum and lung at different time, and the effects of anisodamine (654-2) treatment in rats with oleic acid-induced ARDS. METHODS: The ARDS model induced by intravenous injection of oleic acid in the rat was used and levels of IL-6, IL-8, TNF-? in serum and lung tissue supernatant were measured using enzyme linked immunosorbent assay (ELISA). RESULTS: Levels of serum and lung tissue IL-6, IL-8, TNF-? in oleic acid type ARDS 4 h group were increased significantly. These cytokines in oleic acid type ARDS 8 h group were lower than that of ARDS 4 h group, but serum IL-6, TNF-? and lung tissue IL-6 were still higher than that of control group . In oleic acid type ARDS 16 h group, serum IL-6, TNF-? were lower than that of the ARDS 8 h group and serum TNF-? and lung tissue IL-6 were higher than that of control group. After 654-2 treatment, the levels of serum and lung tissue IL-6, TNF-? were decreased significantly. CONCLUSION: IL-6, IL-8 and TNF-? might play important roles in the oleic acid-induced ARDS in the rat. 654-2 might alleviate ARDS by inhibiting excess production of IL-6 and TNF-?.
ABSTRACT
AIM: To observe the dynamic changes of interleukin-4(IL-4),IL-10,IL-12 in rat serum and lung tissues during acute respiratory distress syndrome (ARDS). METHODS: The ARDS model of rats was induced by intravenous injection of oleic acid. The levels of IL-4 ,IL-10,IL-12 in serum and the supernatant of lung tissues were measured by enzyme linked immunosorbent assay (ELISA). RESULTS: The Levels of serum and lung IL-10,IL-12 in ARDS rats were increased in 4 h ,8 h,16 h group compared with control group . The levels in IL-10 in serum in 16 h group and IL-10 in lung tissues of 8 h group were lower than that in 4 h group. The Levels of IL-4 in serum in 4 h, 8 h group were higher than that in control group , while IL-4 in 16 h group was lower than that in 8 h group. IL-4 of lung tissues in 4 h,8 h,16 h group were increased significantly,but in 16 h group were lower than that in 8 h group. The biggest changes of pulmonary coefficient and histopathology were observed at 4 h after injection of oleic acid. CONCLUSIONS: IL-4,IL-10 and IL-12 might play important roles in inflammatory reaction induced by oleic acid. The pro- and anti-inflammatory cytokines produced successively during ARDS. The relationship between unbalanced cytokines and lung injury in ARDS needs to be further studied.