Annexin1 regulates the erythroid differentiation through ERK signaling pathway.
K562 cells can be used as a model of erythroid differentiation on being induced by hemin. We found that the level of annexin1 gene expression was notably increased during this indicated process. To test the hypothesis that annexin1 can regulate erythropoiesis, K562 cell clones in which annexin1 was stably increased and was knocked down by RNAi were established, respectively. With analysis by hemoglobin quantification, benzidine staining, and marker gene expression profile determination, we confirmed that hemin-induced erythroid differentiation of K562 cells was modestly stimulated by overexpression of annexin1 while it was significantly blocked by knock down of annexin1. Further studies revealed that the mechanisms of annexin1 regulation of the erythroid differentiation was partially related to the increased ERK phosphorylation and expression of p21(cip/waf), since specific inhibitor of MEK blocked the function of annexin1 in erythroid differentiation. We concluded that annexin1 exerted its erythropoiesis regulating effect by ERK pathway.
Huo
Xiao-fang
XF
National Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, The Chinese Academy of Medical Sciences and The Peking Union Medical College, 5 Dong Dan San Tiao, Beijing 100005, People's Republic of China.
Zhang
Jun-Wu
JW
D017305:Annexin A1 / Q000502:physiology*; D015152:Blotting, Northern; D002454:Cell Differentiation / Q000502:physiology*; D004920:Erythropoiesis; D006801:Humans; D020014:K562 Cells; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000502:physiology*
D017305:Annexin A1; D020928:Mitogen-Activated Protein Kinases