[Role of Rictor in Hematopoietic Stem Cells during Fetal Liver Hematopoiesis].

OBJECTIVE: To investigate the effect of Rictor on the hematopoiesis of fetal liver by specific knock-out of Rictor in hematopoietic cells of Vav-Cre mice. METHODS: E12.5 0.08ee fetal liver cells from the experimental group Vav-Cre; Rictorf/f embryos and control group Rictor f/+ or Rictorf/f embryos were transplanted to recipients respectively to observe the effect of Rictor on reconstitution ability of hematopoietic stem cells. In the meantime, E14.5 0, 10, 20, 40, 60, 80 sorted hematopoietic stem cells from the Vav-Cre; Rictorf/f fetal liver of experimental group and Rictorf/+ or Rictorf/f fetal liver of control group were transplanted in to recipients to analyze the numbers of functional hematopoietic stem cells after Rictor was knocked-out. Furthermore, the self-renewal capacity was investigated by secondary transplantation of BM cells from primary recipients that had been successfully repopulated with E12.5 fetal liver-derived cells and by cell cycle analysis. RESULTS: All the recipients receiving E12.5 Rictorf/+ or Rictorf/f cells were repopulated (8/8, from 2 independent experiments) with an average chimerism of 77.2%±11.1% at 4 months post-transplantation, which resulted in 57 LT-RU per FL. In comparison, 8 out of 8 recipients receiving Vav-Cre; Rictorf/f cells were repopulated with significantly reduced chimerism (37.0%±16.3%) (P＜0.01), which was equivalent to 8 LT-RU per FL. The limiting dilution transplantation experiment showed that there was one functional hematopoietic stem cell out of 17 sorted SLAM cells in the control group, and one functional hematopoietic stem cell out of 39 sorted SLAM cells in the experimental group. The secondary transplantation experiments showed that 2 out of 4 recipients were reconstructed in the control group after 1 month, and 0 was reconstructed in the experimental group by transplanting 4×105 donor cells respectively. What＇s more, the percentage of S/G2/M cells in the experimental group increased when compared with controls. CONCLUSION: In the process of fetal liver hematopoiesis, the specifically knocking-out the Rictor in hematopoietic system can lead to defect of reconstitution ability, decrease of the functional hematopoietic stem cell numbers and reduction of self-renewal ability of hematopoietic stem cells.

[CatSper in sperm hyperactivation and male infertility: Advances in studies].

The CatSper channel is known as one of the most important Ca²âº channels on the cell membrane of mammalian sperm and plays a key role in the motility, hyperactivation and fertilization function of sperm. The CatSper protein, expressed exclusively in the principal piece of the sperm tail, is composed of CatSper1-4 and 5 auxiliary unitsß,γ,δ and ε, and has an essential part in the functional and structural domains of Ca²âºas well as in the spatiotemporal regulation of the P-Tyr protein, sperm hyperactivation, efficient sperm migration in the oviduct, egg penetration, and normal fertility. Recent studies show that functional deficiency of CatSper seriously affects sperm function,and the loss of any one of its 9 subunits may lead to male reproductive dysfunction. This paper outlines recent advances in the studies of the CatSperprotein, focusing on its expression, location, structure, and regulation,as well as itsinfluence on sperm hyperactivation and male reproduction.

[Role of NF-κB inhibitor in Acute Myeloid Leukemia].

OBJECTIVE: To investigate the role of NF-κB inhibitor in occurence and development of AML. METHODS: AML and normal bone marrow samples were collected from 8 AML patients and 8 normal persons. The expression of NF-κB signaling pathway genes was detected by NF-κB PCR array. Then, AML mouse model was constructed to test the role of NF-κB inhibitor in AML. RESULTS: The NF-κB signal pathway was activated in AML patients. The up-regulated genes, EDARADD, TNFSF14, could activate the NF-κB signal pathway, IL6 could regulate the inflammatory signal. The down-regulated genes, TNFRSF 10B, TNFRSF1A, could lead to cell apoptosis. the AML mouse model was constructed successfully. Then administration of NF-κB inhibitor reduced the inhibition of leukemia niche to the normal hematopoietic stem cells (HSCs), promoted the HSC to enter into cell cycle. CONCLUSION: The NF-κB signal pathway is activated in AML cells. AML mouse model is constructed successfully. NF-κB inhibitor has a potential to treat AML and promotes the HSC to enrter into cell cycle.