The authors profiled transcriptomes of blood vascular endothelial cells from peripheral lymph nodes and map phenotypes to the vasculature.
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Brulois, K., Rajaraman, A., Szade, A., Nordling, S., Bogoslowski, A., Dermadi, D., Rahman, M., Kiefel, H., O’Hara, E., Koning, J. J., Kawashima, H., Zhou, B., Vestweber, D., Red-Horse, K., Mebius, R. E., Adams, R. H., Kubes, P., Pan, J., & Butcher, E. C. (2020). A molecular map of murine lymph node blood vascular endothelium at single cell resolution. Nature Communications, 11(1), 1–15. https://doi.org/10.1038/s41467-020-17291-5 Cite
Mechanistically, RNA sequencing revealed that resolvin D1 induced a transcriptional program in macrophages characteristic of a pro-revascularization phenotype. Vascularization of ischemic skeletal muscle, as well as cutaneous wounds, was impaired in mice with myeloid-specific deficiency of Alx/Fpr2, and this was associated with altered expression of pro-revascularization genes in skeletal muscle and macrophages isolated from skeletal muscle.
[Proceedings of the National Academy of Sciences of the United States of America]
Euscaphic acid protected vascular endothelial cells against hypoxia-induced apoptosis via ERK1/2 signaling pathway, and tormentic acid brought its efficacy into full play via PI3K/AKT and ERK1/2 signaling pathways.
Scientists explored the inherent mechanism of lncRNA OIP5-AS1 in hepatocellular carcinoma (HCC). In the first place, qRT-PCR found that OIP5-AS1 and VEGFA expressions were significantly increased while miR-3163 was obviously reduced in HCC cells and tissues.
[Cancer Biology & Therapy]
Using acute myeloid leukemia (AML) mouse models, scientists showed AML blasts released inflammatory mediators that upregulated endothelial niche E-selectin expression.