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STAT3 信号通路在人急性单核细胞白血病细胞向树突状细胞分化中的作用及机制探讨
- Source :
-
Shandong Medical Journal . 3/16/2018, Vol. 58 Issue 10, p1-4. 4p. - Publication Year :
- 2018
-
Abstract
- Objective To detect the role and mechanisms of signal transducers and activators of transcription 3(STAT3) in promoting the differentiation of human acute monocytic leukemia eells into dendritic cells(DCs). Methods Human acute monocytic leukemia cells THP-1 were randomly divided into two groups: the observation group and the control group. Cells in the observation group were induced to differentiate into DCs by granulocyte-macrophage colony stimulating factor (GM-CSF) combined with interleukin-4 (IL-4), and we used Lipopolysaccharide (LPS) to induce THP-1-derived DC maturation; cells in the control group were not treated. The cells in the two groups were collected on day 7 of culture, the morphologic features were observed under inverted microscope; DC surface marker CDlle and DC surface functional molecules(CD80, HLA-DR, and CCR7) were detected by flow cytometry; the mRNA expression of STAT3 and E2-2 was detected by q-PCR; in addition, the protein expression of STAT3 and phosphorylation (p-STAT3) was detected by Western blotting. Results The cells in the control group showed a round shape and uniform morphology. After cytokines induction, obvious morphological changes of DCs were observed. Compared with the control group, the DC surface marker CD11c and DC surface functional molecules of the observation group were higher, and both the mRNA expression levels of STAT3 and E2-2 and the protein expression levels of STAT3 and p-STAT3 increased signifieandy (all Pc 0.05). Conclusion During the differentiation of THP-1 cells into DCs induced by GM-CSF and IL-4 , STAT3 signaling pathway activates specific nuclear transcription factor E2-2 , which in turn induces the differentiation of THP-1 into DCs. [ABSTRACT FROM AUTHOR]
Details
- Language :
- Chinese
- ISSN :
- 1002266X
- Volume :
- 58
- Issue :
- 10
- Database :
- Academic Search Index
- Journal :
- Shandong Medical Journal
- Publication Type :
- Academic Journal
- Accession number :
- 128953840
- Full Text :
- https://doi.org/10.3969/j.issn.1002-266X.2018.10.001