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Chinese Journal of Pathophysiology ; (12): 1863-1869, 2016.
Article in Chinese | WPRIM | ID: wpr-504013

ABSTRACT

[ ABSTRACT] AIM:To investigate the expression relevance of transcription factors GATA-1 and GATA-2 in the bone marrow CD71 +cells of a high-altitude polycythemia (HAPC) rat model.METHODS:Male SD rats (n=48) were randomly divided into normal control group and HAPC model group .HAPC model was established at an altitude of 4 300 m in the natural environment and verified by the morphology and quantity of the bone marrow cells and hematologic parameters detection .A relative change in the trend of bone marrow CD 71 +cell numbers was detected by flow cytometry analysis .The expression of GATA-1 and GATA-2 at mRNA and protein levels in the CD 71 +cells was examined by RT-qPCR and West-ern blot .CD71 +cells were cultured under hypoxic condition and transfected with the optimal interference sequence of GA -TA-1shRNA1 for 96 h.The expression of GATA-1 and GATA-2 at mRNA and protein levels was detected by RT-qPCR and Western blot .RESULTS:The establishment of the animal model with HAPC was successful as the bone marrow smears and the hematologic parameters showed compared with the control .The quantity of the bone marrow CD 71 +cells of HAPC rats were significantly increased and the expression of GATA-1 at mRNA and protein levels in the CD 71 +cells were higher than those of the control .The expression of GATA-2 at mRNA and protein levels was similar to that of the control .The correla-tion analysis showed that the expression of GATA-1 was negatively correlated with that of GATA-2 in the control, while no obvious correlation between them was observed in the HAPC rats .The expression of GATA-1 at mRNA and protein levels in HAPC group was lower than that in control group after interfered by GATA-1 shRNA1 for 96 h, but no obvious diversity of GATA-2 expression between the 2 groups was observed .CONCLUSION:GATA-1 and GATA-2 are abnormally expressed and their negative correlation is destroyed in HAPC , which may be one of the pathogenesis of HAPC .

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