scholarly journals Tumor necrosis factor receptor type 1-associated death domain (TRADD) regulates epithelial-mesenchymal transition (EMT), M1/M2 macrophage polarization and ectopic endometrial cysts formation in endometriosis

2021 ◽  
Vol 9 (2) ◽  
pp. 148-148
Author(s):  
Chang Lu ◽  
Yong Liu ◽  
Xiaodan Wang ◽  
Haili Jiang ◽  
Zhaohui Liu
Keyword(s):  
Tumor Necrosis ◽  
Epithelial Mesenchymal Transition ◽  
Macrophage Polarization ◽  
Tumor Necrosis Factor Receptor ◽  
M2 Macrophage ◽  
Death Domain ◽  
Mesenchymal Transition ◽  
M2 Macrophage Polarization ◽  
Necrosis Factor

scholarly journals Exosomal DLX6-AS1 from hepatocellular carcinoma cells induces M2 macrophage polarization to promote migration and invasion in hepatocellular carcinoma through microRNA-15a-5p/CXCL17 axis

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Lin-pei Wang ◽  
Jing Lin ◽  
Xiao-qiu Ma ◽  
Dong-yao Xu ◽  
Chun-feng Shi ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Macrophage Polarization ◽  
Migration And Invasion ◽  
M2 Macrophage ◽  
M2 Macrophages ◽  
Mesenchymal Transition ◽  
M2 Macrophage Polarization ◽  
Hcc Cells

Abstract Background Hepatocellular carcinoma (HCC) cells-secreted exosomes (exo) could stimulate M2 macrophage polarization and promote HCC progression, but the related mechanism of long non-coding RNA distal-less homeobox 6 antisense 1 (DLX6-AS1) with HCC-exo-mediated M2 macrophage polarization is largely ambiguous. Thereafter, this research was started to unearth the role of DLX6-AS1 in HCC-exo in HCC through M2 macrophage polarization and microRNA (miR)-15a-5p/C-X-C motif chemokine ligand 17 (CXCL17) axis. Methods DLX6-AS1, miR-15a-5p and CXCL17 expression in HCC tissues and cells were tested. Exosomes were isolated from HCC cells with overexpressed DLX6-AS1 and co-cultured with M2 macrophages. MiR-15a-5p/CXCL17 down-regulation assays were performed in macrophages. The treated M2 macrophages were co-cultured with HCC cells, after which cell migration, invasion and epithelial mesenchymal transition were examined. The targeting relationships between DLX6-AS1 and miR-15a-5p, and between miR-15a-5p and CXCL17 were explored. In vivo experiment was conducted to detect the effect of exosomal DLX6-AS1-induced M2 macrophage polarization on HCC metastasis. Results Promoted DLX6-AS1 and CXCL17 and reduced miR-15a-5p exhibited in HCC. HCC-exo induced M2 macrophage polarization to accelerate migration, invasion and epithelial mesenchymal transition in HCC, which was further enhanced by up-regulated DLX6-AS1 but impaired by silenced DLX6-AS1. Inhibition of miR-15a-5p promoted M2 macrophage polarization to stimulate the invasion and metastasis of HCC while that of CXCL17 had the opposite effects. DLX6-AS1 mediated miR-15a-5p to target CXCL17. DLX6-AS1 from HCC-exo promoted metastasis in the lung by inducing M2 macrophage polarization in vivo. Conclusion DLX6-AS1 from HCC-exo regulates CXCL17 by competitively binding to miR-15a-5p to induce M2 macrophage polarization, thus promoting HCC migration, invasion and EMT.

The Role of Tumor Necrosis Factor Receptor Type 1 in Orthodontic Tooth Movement

2007 ◽  
Vol 86 (11) ◽  
pp. 1089-1094 ◽  
Author(s):  
I. Andrade ◽  
T.A. Silva ◽  
G.A.B. Silva ◽  
A.L. Teixeira ◽  
M.M. Teixeira
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tooth Movement ◽  
Tumor Necrosis Factor Receptor ◽  
Orthodontic Tooth Movement ◽  
Receptor Type ◽  
Periodontal Tissues ◽  
Tnf Α ◽  
Necrosis Factor

Orthodontic tooth movement is dependent on osteoclast activity. Tumor necrosis factor (TNF)-α plays an important role, directly or via chemokine release, in osteoclast recruitment and activation. This study aimed to investigate whether the TNF receptor type 1 (p55) influences these events and, consequently, orthodontic tooth movement. An orthodontic appliance was placed in wild-type mice (WT) and p55-deficient mice (p55−/−). Levels of TNF-α and 2 chemokines (MCP-1/CCL2, RANTES/CCL5) were evaluated in periodontal tissues. A significant increase in CCL2 and TNF-α was observed in both groups after 12 hrs of mechanical loading. However, CCL5 levels remained unchanged in p55−/− mice at this time-point. The number of TRAP-positive osteoclasts in p55−/− mice was significantly lower than that in WT mice. Also, there was a significantly smaller rate of tooth movement in p55−/− mice. Analysis of our data suggests that the TNFR-1 plays a significant role in orthodontic tooth movement that might be associated with changes in CCL5 levels.

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