RESUMEN
Objective To investigate the relationship of Maternal-fetal interface local cytokine GM-CSF and its receptor with the occurrence of early spontaneous abortion. Methods From August 2009 to December 2011,we collected 30 villi tissue samples with artificial abortion and 30 villi tissue samples with spontaneous abortion. At the same time, we collected 30 villi tissue samples with artificial abortion and 30 decidua tissue samples with spontaneous abortion,and 30 decidua tissue samples with spontaneous abortion. The human chorionic gonadotropin ( HCG) was detected by radioimmunoassay in every group. The expressions of granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte-macrophage colony-stimulating factor receptor (GM-CSFR ) were detected by Immunohistochemical staining and Western Blot in the villi tissue and decidua tissue in every group. Results The concentration of HCG in the spontaneous abortion group was lower than that in the artificial abortion group ( <0.05) . The protein expressions of GM-CSF and GM-CSFR were found in villus and deciduas tissues in both groups. The protein expression levels of GM-CSFR in the villus tissues were higher in spontaneous abortion group than those in artificial abortion group ( <0.05), the protein expression of GM-CSF was upregulated, but there was no statistically significant difference between two groups. In deciduas tissues, the protein expressions of GM-CSF and GM-CSFR were upregualted in spontaneous abortion group ( <0.05) . Conclusions The suitable concentrations of GM-CSF and GM-CSFR in decidua tissue maintain the pregnancy continued. However,the higher concentrations of GM-CSF and GM-CSFR in the decidua tissue may be one of reasons of spontaneous abortion.
RESUMEN
Objective To explore the effect of macrophage colony stimulating factor (M-CSF) on lung cancer cell line A549. Methods After M-CSF at 0.1, 1 and 10 ng/ml was given to cultured A549 cells for 0, 24, 48, 72 and 92 h respectively, their morphological changes were observed with inverted microscopy, proliferation was measured by MTT assay, and cell cycles were determined by flow cytometry. RT-PCR was used to detect the change of expression of M-CSF receptor. Result The growth of A549 was significantly inhibited by M-CSF in a concentration- and time- dependent manner. The maximum response was obtained at 10 ng/ml of M-CSF. Flow cytometric analysis revealed that the treated A549 cells arrested at the G0/G1 phase of the cell cycle. RT-PCR showed that the mRNA expression of M-CSF receptor was reduced after the M-CSF treatment. Conclusion M-CSF has an anti-tumour activity on lung cancer cell A549.