mProX™ Human CMKLR1 Stable Cell Line

Mayer S, et al. "The tumor microenvironment shows a hierarchy of cell-cell interactions dominated ." Nature communications, 2023.
The tumor microenvironment (TME) is a complex network of non-malignant cells that play a crucial role in cancer biology. To understand this complexity, researchers have developed an experimental-mathematical approach to break down the TME into smaller circuits of interacting cell types. Through the analysis of single-cell RNA sequencing data from female breast cancer patients, a hierarchical network of interactions was identified, with cancer-associated fibroblasts (CAFs) at the top secreting factors mainly towards tumor-associated macrophages (TAMs). By isolating the strongest two-cell circuit motif in vitro, researchers were able to mimic the hierarchy of in vivo interactions and test the effect of specific ligand-receptor interactions on cell dynamics and function. This approach led to the discovery of a mediator of CAF-TAM interactions, RARRES2, and its receptor CMKLR1. This study highlights the importance of identifying small circuits within the TME in simplifying its complexity and developing potential strategies to modify its function.
Pubmed: 37726308   DOI: 10.1038/s41467-023-41518-w

Hernandez J, et al. "n-3 Polyunsaturated Fatty Acids Modulate LPS-Induced ARDS and the Lung-Brain Axis ." International journal of molecular sciences, 2023.
Specialized pro-resolving mediators (SPMs) and specifically Resolvin E1 (RvE1) have been found to effectively terminate inflammation and aid in healing during lung diseases like acute respiratory distress syndrome (ARDS). Despite primarily affecting the lungs, many ARDS patients also experience neurocognitive impairments. In order to explore the correlation between the lung and brain during ARDS and the potential therapeutic use of SPMs and its derivatives, experiments were conducted on fat-1 mice bred with RvE1 receptor knockout mice. ARDS was induced using lipopolysaccharide (LPS, 10 microg) administered through the intratracheal route. Mice were sacrificed at 0 h, 4 h, 24 h, 72 h, and 120 h following inflammation, and various assessments including RT-PCR, multiplex, immunohistochemistry, Western blot, and LC-MS/MS were performed to gauge the effects on the lung, liver, and brain. RT-PCR and protein analysis revealed a raise in inflammatory signaling in the hypothalamus, despite low signaling in the peripheral regions, due to inflammation triggered by LPS. Immunohistochemical staining was able to determine neutrophil recruitment in multiple brain structures. This study shows that during ARDS, immune cells go through the brain, interfacing with the immune system rather than using cytokines. Furthermore, the absence of RvE1 receptors along with heightened levels of omega-3 polyunsaturated fatty acids in fat-1 mice changed the interactions between the lung and brain during ARDS by modifying the levels of various inflammatory and lipid mediators as well as glial activity markers.
Pubmed: 37686333   DOI: 10.3390/ijms241713524