J W Zhao1, G Shi, J D Ping, L Ming. 1. Clinical Laboratory, the First Affiliated Hospital of Zhengzhou University, Key Clinical Laboratory of Henan Province, Zhengzhou 450052, China.
Abstract
Objective: To investigate the expression of tumor necrosis factor alpha-inducible protein 8 like-2 (TIPE2) and tissue factor (TF) in patients with bronchial asthma. And to explore the regulation of TIPE2 on TF. Methods: Sixty-five asthmatic patients and 40 healthy controls were selected from the First Affiliated Hospital of Zhengzhou University from July to November, 2017. The expression of TIPE2 and TF in peripheral blood mononuclear cells of asthmatic patients and healthy controls were detected by Western blot.The level of TF protein in plasma was detected by enzyme-linked immunosorbent assay. The changes of TIPE2 and TF mRNA expression in THP-1 cells stimulated by house dust mite extract were detected by real-time fluorescence quantitative PCR (RT-PCR). The recombinant adenovirus Adv-TIPE2 was constructed and transfected into THP-1 cells and the effect of over-expression TIPE2 on TF expression in THP-1 cells was detected by RT-PCR. Results: The relative level of TIPE2 protein in asthmatic patients and healthy controls was 0.025±0.010 and 0.087±0.070, while that of TF was 0.40±0.27 and 0.15±0.10, respectively. Compared with healthy controls, the levels of TIPE2 protein decreased and TF protein increased in asthmatic patients, the differences were statistically significant (t=-5.06, 9.04, P<0.05) . TIPE2 protein level was negatively correlated with TF protein level (r=-0.460 3, P<0.05). The house dust mite extract reduced the expression level of TIPE2 mRNA in THP-1 cells, but increased the level of TF mRNA expression. When the concentration was 1 μg/ml, the change of TIPE2 mRNA was the most obvious at 4 h (P<0.05). The recombinant adenovirus Adv-TIPE2 was successfully constructed. The level of TF mRNA expression in THP-1 cells over-expressing TIPE2 gene was reduced (P<0.05). Conclusion: TIPE2, a negative regulator of inflammation, has a negative control effect on TF, and may be involved in the hyper-coagulable state of bronchial asthma by regulating TF expression.
Objective: To investigate the expression of tumor necrosis factor alpha-inducible protein 8 like-2 (TIPE2) and tissue factor (TF) in patients with bronchial asthma. And to explore the regulation of TIPE2 on TF. Methods: Sixty-five asthmatic patients and 40 healthy controls were selected from the First Affiliated Hospital of Zhengzhou University from July to November, 2017. The expression of TIPE2 and TF in peripheral blood mononuclear cells of asthmatic patients and healthy controls were detected by Western blot.The level of TF protein in plasma was detected by enzyme-linked immunosorbent assay. The changes of TIPE2 and TF mRNA expression in THP-1 cells stimulated by house dust mite extract were detected by real-time fluorescence quantitative PCR (RT-PCR). The recombinant adenovirus Adv-TIPE2 was constructed and transfected into THP-1 cells and the effect of over-expression TIPE2 on TF expression in THP-1 cells was detected by RT-PCR. Results: The relative level of TIPE2 protein in asthmatic patients and healthy controls was 0.025±0.010 and 0.087±0.070, while that of TF was 0.40±0.27 and 0.15±0.10, respectively. Compared with healthy controls, the levels of TIPE2 protein decreased and TF protein increased in asthmatic patients, the differences were statistically significant (t=-5.06, 9.04, P<0.05) . TIPE2 protein level was negatively correlated with TF protein level (r=-0.460 3, P<0.05). The house dust mite extract reduced the expression level of TIPE2 mRNA in THP-1 cells, but increased the level of TF mRNA expression. When the concentration was 1 μg/ml, the change of TIPE2 mRNA was the most obvious at 4 h (P<0.05). The recombinant adenovirus Adv-TIPE2 was successfully constructed. The level of TF mRNA expression in THP-1 cells over-expressing TIPE2 gene was reduced (P<0.05). Conclusion:TIPE2, a negative regulator of inflammation, has a negative control effect on TF, and may be involved in the hyper-coagulable state of bronchial asthma by regulating TF expression.