CXC Chemokine Receptor 4 (CXCR4) Antagonist, a Novel Pathway to Prevent Chronic Allograft Nephropathy

2016 ◽  
Vol 21 ◽  
pp. 728-734 ◽  
Author(s):  
Yue Xu ◽  
Qiang Zhang ◽  
Wenrui Xue ◽  
Song Zeng ◽  
Zijian Zhang ◽  
...  
2015 ◽  
Vol 308 (8) ◽  
pp. G702-G709 ◽  
Author(s):  
Gregory C. Wilson ◽  
Christopher M. Freeman ◽  
Joshua W. Kuethe ◽  
Ralph C. Quillin ◽  
Hiroyuki Nojima ◽  
...  

The role of stromal cell-derived factor-1 (SDF-1 or CXCL12) and its receptor CXC chemokine receptor-4 (CXCR4) in ischemic liver injury and recovery has not been studied. Some reports suggest that this chemokine may aid in liver regeneration, but others suggest that it may be profibrotic through its activation of hepatic stellate cells. In this study we sought to elucidate the role of SDF-1 and its receptor CXCR4 during liver injury, recovery, and regeneration after ischemia-reperfusion (I/R). A murine model of partial (70%) I/R was used to induce liver injury and study the reparative and regenerative response. CXCR4 was expressed constitutively in the liver, and hepatic levels of SDF-1 peaked 8 h after reperfusion but remained significantly increased for 96 h. Treatment of mice with the CXCR4 antagonist AMD3100 or agonist SDF-1 had no effect on acute liver injury assessed 8 h after I/R. However, treatment with AMD3100 increased hepatocyte proliferation after 72 and 96 h of reperfusion and reduced the amount of liver necrosis. In contrast, treatment with SDF-1 significantly decreased hepatocyte proliferation. These effects appeared to be dependent on the presence of liver injury, as AMD3100 and SDF-1 had no effect on hepatocyte proliferation or liver mass in mice undergoing 70% partial hepatectomy. The data suggest that signaling through CXCR4 is detrimental to liver recovery and regeneration after I/R and that clinical therapy with a CXCR4 antagonist may improve hepatic recovery following acute liver injury.


2007 ◽  
Vol 56 (10) ◽  
pp. 1589-1595 ◽  
Author(s):  
Stefania Scala ◽  
Caterina Ieranò ◽  
Alessandro Ottaiano ◽  
Renato Franco ◽  
Anna La Mura ◽  
...  

2017 ◽  
Vol 25 (2) ◽  
pp. 646-657 ◽  
Author(s):  
Markus Baumann ◽  
Mohammad Musarraf Hussain ◽  
Nina Henne ◽  
Daniel Moya Garrote ◽  
Stefanie Karlshøj ◽  
...  

Nanoscale ◽  
2021 ◽  
Author(s):  
Shanta Bhattarai ◽  
Yuri Mackeyev ◽  
Bhanu Venkatesulu ◽  
Sunil Krishnan ◽  
Pankaj Kumar Singh

CXC chemokine receptor 4 (CXCR4) is overexpressed on most breast cancer cell surfaces including triple negative breast cancer (TNBC) which lacks traditional receptor overexpression. We targeted gold nanoparticles (GNPs) to...


Planta Medica ◽  
2020 ◽  
Vol 86 (05) ◽  
pp. 331-337
Author(s):  
Buyun Kim ◽  
Yu-Hong Min ◽  
Byoungduck Park

AbstractMetastasis, which is closely linked to cancer-related deaths, is a highly complex process. It is an organ-specific process and involves interactions between the host and cancer cells. CXC chemokine receptor 4 is known to be expressed in various tumors and the binding with CXC ligand 12 induces signaling in cancer cell survival, migration, and proliferation. Particularly, the CXC chemokine receptor 4/CXC ligand 12 axis is known to promote the metastasis of breast cancer. Thus, agents that can downregulate CXC chemokine receptor 4 expression have potential against cancer metastasis. Minecoside is an active compound extracted from Veronica peregrina L. It is widely distributed in Korea and has been used as a traditional drug for the treatment of various chronic diseases. However, the anticancer and anti-inflammatory effects of minecoside have yet to be clarified. In this study, we found that minecoside downregulates constitutive CXC chemokine receptor 4 expression in MDA-MB-231 breast cancer cells. This downregulation also occurred at the transcriptional level. Minecoside-mediated suppression of CXC chemokine receptor 4 expression inhibited CXC ligand 12-induced invasion of breast and colorectal cancer cells. Overall, our results suggest that minecoside can be a novel anticancer agent that can inhibit cancer metastasis through inhibition of CXC chemokine receptor 4 expression.


Medicine ◽  
2019 ◽  
Vol 98 (23) ◽  
pp. e15948 ◽  
Author(s):  
Tingyong Cao ◽  
Yuanxin Ye ◽  
Hongyan Liao ◽  
Xiao Shuai ◽  
Yongmei Jin ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document