[Increased expression of transendothelial migration-related molecules CCL4, ICAM-1 and VCAM-1 in lung tissue after surgical removal of mouse tumor-bearing lymph node].

Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology(2020)

引用 1|浏览17
暂无评分
摘要
Objective To detect the expression of chemokine and adhesion molecules related to leukocytes' transendothelial migration, meanwhile, to investigate changes of reticular fibers and the expression of vimentin and matrix metalloproteinase-9 (MMP9) in lung tissues after surgical removal of mouse tumor-bearing lymph node, revealing their changes and roles in the formation of pre-metastatic microenvironment in the lung. Methods B16F10 melanoma cells were inoculated into mouse subiliac lymph node (SiLN). Twenty mice were equally divided into groups with or without (as a control group) tumor-bearing SiLN removal. Fifteen days later, tumor-bearing lymph node was surgically removed; 3 days after resection, mouse lung tissues were collected. The change of reticular fibers in lung tissues was observed by silver impregnation staining. The expression of C-C motif chemokine ligand 4 (CCL4), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), vimentin and MMP9 in lung tissues was detected by Western blotting. Results Compared with control group, expression of MMP9 and vimentin increased significantly in the lung tissues of SiLN removal group; reticular fibers were obviously fractured and its per area was reduced. Moreover, expression of CCL4, ICAM-1 and VCAM-1 also significantly increased. Conclusion Expression of CCL4, ICAM-1, VCAM-1, MMP9 and vimentin in mouse lung tissues is promoted after surgical removal of tumor-bearing lymph node, contributing to inflammatory cells' adhesion to and extravasation across vascular endothelium and further resulting in the formation of inflammatory microenvironment.
更多
查看译文
关键词
molecules ccl4,lung tissue,lymph node,migration-related,tumor-bearing
AI 理解论文
溯源树
样例
生成溯源树,研究论文发展脉络
Chat Paper
正在生成论文摘要