Rat MCP-1 ELISA Kit

Radiotherapy is mainly a traditional treatment for breast cancer; however, the key genes and pathways in breast cancer associated with irradiation are not clear. In this study, we aimed to explore the messenger RNA expression changes between preradiation and postradiation breast cancer. The gene expression data set (GSE59733) was downloaded from Gene Expression Omnibus database. According to |log(2)FC (fold change) | >= 1 and with false discovery rate adjustedPvalue <.05, differentially expressed genes (DEGs) were screened and annotated by R programming software. The protein-protein interaction (PPI) network was conducted through STRING database, and subnetworks and hub genes were extracted by plug-in in Cytoscape. A total of 82 DEGs (74 upregulated and 8 downregulated genes) were identified. These DEGs mainly enriched in an intrinsic apoptotic signaling pathway and G-protein-coupled receptor binding. What's more, tumor necrosis factor signaling pathway and interleukin 17 signaling pathway abnormally activated in postradiation tumor samples. Two characteristic subnetworks and 3 hub genes (FOS,CCL2, andCXCL12) were strongly distinguished in PPI network. Moreover, the expression level of the hub genes was confirmed in irradiated MCF-7 cell and SUM-159 cell using quantitative real-time polymerase chain reaction assay. These findings imply that these hub genes may play momentous function in breast cancer to irradiation.

Mucins have long been regarded to play a role as a barrier to prevent mucosal infections; however, some studies report that overexpression of mucins induces obstruction and inflammation of airways. We investigated whether the secretion of overexpressed mucin, mucin5ac (MUC5AC), could improve protection against pathogens. To examine the possible roles of mucin hypersecretion in augmenting host defense against disease-promoting muco-obstructive lung disease, a mouse model that overexpressed MUC5AC was generated. We had previously proved that murine gammaherpesvirus-68 (MHV-68) infection could induce emphysema in mice, which later developed into combined pulmonary fibrosis and emphysema (CPFE). We further explored whether increased MUC5AC secretion could provide benefits against MHV-68 induced fibrosis. We initially developed a pcDNA3.1-MUC5AC mouse model. Next, the experimental mice were randomly divided into five groups: normal control, pcDNA3.1 control, pcDNA3.1-MUC5AC, CPFE, and pcDNA3.1- MUC5AC + CPFE. Morphometric analysis of each group was performed by hematoxylin and eosin staining and Masson trichrome staining. MUC5AC levels in lung tissues were analyzed by immunohistochemical staining, real-time polymerase chain reaction, and Western blot analysis. The airway inflammation was determined by differential cell counts of bronchoalveolar lavage fluid (BALF) and measurement of cytokines and chemokines in BALF by enzyme-linked immunosorbent assay. MUC5AC hypersecretion alone was not sufficient to drive goblet cell metaplasia to induce obvious mucus plugging and airway inflammation. However, MUC5AC overexpression served as a protective barrier against MHV-68 virus infection in vivo. Infectivity of MHV-68 was decreased in the pcDNA3.1-MUC5AC + CPFE group compared with that in CPFE group. Meanwhile, a reduction of MHV-68 virus attenuated the expressions of chemokine (C-C motif) ligand 2 (CCL2), chemokine (C-X-C motif) ligand 5 (CXCL5), interleukin-13 (IL-13), and transforming growth factor-beta 1 (TGF-beta 1), and weakened airway inflammation and fibrosis in the pcDNA3.1-MUC5AC + CPFE group. Overexpression of MUC5AC appears to exhibit a protective role against MHV-68 infection in mice with emphysema that subsequently developed into CPFE and to further decrease airway inflammation and fibrosis induced by MHV-68 by decreasing the expressions of CCL2, CXCL5, IL-13, and TGF-beta 1.