Relationship between coexpression of EGFR and ERK2 and activation of ERK2 in lung squamous cell carcinomas / 中国病理生理杂志

AIM: To evaluate the relationship between coexpression of EGFR and ERK2 on the level of protein and mRNA and activation of ERK2 in lung squamous cell carcinomas (SCC). METHODS: Twenty cases of lung squamous cell carcinomas and their paired normal lung tissues were studied. The expression of mRNA and protein of EGFR and ERK2 was measured by reverse transcription PCR (RT-PCR) and Western blotting, respectively. The activity of ERK2 was detected by immunoprecipitation and kinase reaction. RESULTS: The results showed that the expression of EGFR mRNA and protein in paired normal lung tissues was hardly detected by RT-PCR and Western blotting, respectively, but in 20 cases of lung SCCs their expression was upregulated significantly. Compared with normal lung tissues, the expression of ERK2 mRNA and protein in lung cancer tissues was also upregulated significantly, the latter increased about 3-5-fold, and the activity of ERK2 in lung SCCs was also markedly activated. CONCLUSIONS: These data highlight that the overexpression of ERK2 and EGFR protein occurs simultaneously in lung SCCs, which mainly results from the increasing level of gene transcription, the increased activity of ERK2 in lung cancer tissues perhaps attributes to the upregulation of coexpression of EGFR and ERK2. [

Change of ICAM-1 expression in intestine tissue of mice induced by LPS and role of p38 MAPK in its expression / 中国病理生理杂志

AIM: To study the change of intercellular adhesion molecule-1(ICAM-1) expression in intestine tissues of mice induced by LPS and regulatory effect of p38 mitogen-activated protein kinase (p38 MAPK) on ICAM-1 expression. METHODS: Protein and mRNA of ICAM-1 were measured using Western blotting and RT-PCR respectively in intestine tissue of BALB/c mice treated by lipopolysaccharide(LPS) or LPS plus SB203580, a specific inhibitor of p38 MAPK. RESULTS: Compared with control group, the expression of ICAM-1 protein and mRNA was increased significantly by LPS stimulation in dose- and time-dependent manner. ICAM-1 expression reached peak value at 12-36 h after LPS stimulation. 20.0 mg/kg of LPS could induce the maximum of ICAM-1 expression. Pretreatment of mice with SB203580 for 30 min could inhibit significantly LPS-induced expression of ICAM-1 protein and mRNA expression in mouse intestine tissues. CONCLUSIONS: These data highlight that LPS could up-regulate ICAM-1 protein and mRNA expression in intestine tissue of mice in dose- and time-dependent manner, and p38 MAPK signal pathway plays an important role in ICAM-1 expression induced by LPS. It suggests that inhibition of p38 MAPK might be a useful principle for the prevention and treatment of intestine damage of endotoxic shock.

Inhibiting role of polydatin to expression of intercellular adhesion molecule-1 induced by lipopolysaccharide on vascular endothelial cells / 中国病理生理杂志

AIM and METHODS: To investigate expression of intercellular adhesion molecule-1(ICAM-1) on human umbilical vein endothelial cells (HUVEC) induced by lipopolysaccharide (LPS) , and inhibiting role of polydatin by cellular immune fluorescent staining and laser confocal microscope scanning technology. RESULTS: Compared with basic expression of ICAM-1 on HUVEC, the ICAM-1 expression was enhanced significantly after stimulated by LPS from 8 h to 36 h, dose-dependent relation appeared between expression of ICAM-1 and LPS. ICAM-1 expression on endothelial cells treated only by polydatin had no abvious change,but inducing role of LPS to expression of ICAM-1 was inhibited significantly by polydatin pretreating endothelial cells. CONCLUSION: The expression of ICAM-1 on endothelial cells can be promoted by LPS , and polydatin can inhibit LPS-induced ICAM-1 expression