Research progress on the negative factors of corneal endothelial cells proliferation

The human corneal endothelium forms a boundary layer between anterior chamber and corneal stoma. The corneal endothelial cells are responsible for maintaining cornea transparency, which is very vital for our visual acuity, via its pump and barrier functions. The adult corneal endothelial cells in vivo lack proliferation in response to the cell loss caused by outer damages and diseases. As a result, in order to compensate for cell loss, corneal endothelial cells migrate and enlarge while not via dividing to increase the endothelial cell density. Therefore, it is not capable for corneal endothelium to restore the corneal clarity. Some researches have proved that in vitro the corneal endothelial maintained proliferation ability. This review describes the current research progress regarding the negative factors that inhibit proliferation of the corneal endothelial cells. This review will mainly present several genes and proteins that inhibit the proliferation of the corneal endothelial cells, of course including some other factors like enzymes and position.     

Acute promyelocytic leukaemia with t(11;17)(q23;q12-21) and a good initial response to prolonged ATRA and combination chemotherapy

Acute myeloid leukaemia (AML) of FAB subtype M3 is associated with t(15;17)(q22;q21) and a relatively good prognosis when treated with all- trans retinoic acid (ATRA) and combination chemotherapy. Rarely, alternative balanced translocations have been described in this subtype of AML. The translocation t(11;17)(q23;q21) leading to a PLZF/RARα rearrangement has been described in a very small number of cases and has been associated with a poor response to ATRA and an adverse prognosis. We describe a case of AML FAB type M3 with this translocation who entered morphological and cytogenetic complete remission after concurrent prolonged ATRA and one course of induction chemotherapy and remains in morphological and molecular remission at 10 months after presentation. This diagnosis therefore may not always be associated with a poor initial response to treatment.     

氧化砷和维甲酸对PLZF-RARa阳性U937细胞的作用

目的：研究氧化砷（As2O3）和全反式维甲酸（AT—RA）对PLZF-RARα阳性细胞的作用。方法：稳定转染PLZF-RARα基因的U937细胞（U937／PLZF）经As2O2、ATRA处理后，Wright—Giemsa染色观察细胞形态，MTr法检测细胞生长增殖状态，流式细胞术（FCM）检测细胞周期和细胞表面分化抗原CD11b、CD64、CD14等的表达变化，荧光免疫细胞化学染色检测融合蛋白表达，细胞化学染色和硝基蓝四氮唑（NBT）还原试验观察细胞功能分化情况。结果：U937／PLZF细胞在去除四环素条件培养后，PLZF—RARα表达明显增加。As2O3（0．51μmol／L）联合ATRA（1μmol／L）使U937／PLZF细胞核质比缩小，核仁减少但未消失；生长增殖受抑；S期细胞减少；CD11b表达增高；PLZF—RARα蛋白表达减弱，分布以胞核弥漫细小颗粒为主。细胞化学染色和NBT反应变化不明显。结论：0．5μmol／L As2O3联合1μmol／LATRA可使PLZF—RARα阳性U937细胞产生轻微的形态学分化趋势，尚不足以引起其发生功能分化。     

Brief homogeneous TCR signals instruct common iNKT progenitors whose effector diversification is characterized by subsequent cytokine signaling

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hCG-PLZF-RARA转基因小鼠发生慢性粒细胞样白血病

目的　为了从整体水平上研究PLZF RARA融合蛋白的致白血病作用 ,建立了仅在髓系细胞中表达PLZF RARA融合基因的转基因小鼠。方法　分子克隆技术构建转基因构件hCG PLZF RARA ,PCR、RT PCR、免疫荧光、骨髓象、病理、维甲酸 (RA)分化试验等进行检测分析。结果　 6只hCG PLZF RARA转基因小鼠发生白血病 ,表现类似人类慢性粒细胞性白血病。组织因子 (tissuefactor,TF)在融合基因表达阳性的小鼠骨髓细胞中有表达 ,而在正常小鼠和融合基因表达阴性的小鼠的骨髓细胞中不表达。结论　PLZF RARA融合基因的表达在白血病的发生中起着极为重要的作用 ,TF受PLZF RARA融合基因表达上调。