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.
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Stem Cell Rev Rep
January 2025
Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101, China.
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Department of Bioengineering, University of Texas at Dallas, Richardson, TX; Department of Biomedical Engineering, UT Southwestern Medical Center, Dallas, TX. Electronic address:
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The L-type Ca channel (Ca1.2) is essential for cardiac excitation-contraction coupling. To contribute to the inward Ca flux that drives Ca-induced-Ca-release, Ca1.
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