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Among the world's leading causes of cardiovascular disease, atherosclerosis is a chronic inflammatory disorder that affects the arteries. Both vasodilation and vasoconstriction, low levels of nitric oxide and high levels of reactive oxygen species and pro-inflammatory factors characterize dysfunctional blood vessels. Hypertension, and atherosclerosis, all start with this dysfunction. Geraniol, a compound of acyclic monoterpene alcohol, found in plants such as geranium, lemongrass and rose, is a primary constituent of essential oils. It shows a variety of pharmacological properties. This study aimed to investigate the impact of geraniol on Ox-LDL-induced stress and inflammation in human umbilical vein endothelial cells. In this study, HUVECs were treated with Ox-LDL or geraniol at different dose concentrations. MTT assay, Western blot, ROS generation and DNA fragmentation were used to evaluate geraniol's effects on Ox-LDL-induced HUVECs inflammation. The results show that geraniol pre-incubation ameliorates Ox-LDL-mediated HUVECs cytotoxicity and DNA fragmentation. The geraniol inhibited the production of pro-inflammatory cytokines by Ox-LDL, including TNF-α, IL-6 and IL-1β. In Ox-LDL-stimulated HUVECs, geraniol suppresses the nuclear translocation and activity of NF-ᴋB as well as phosphorylation of IkBα. Moreover, geraniol activated the PI3K/AKT/NRF2 pathway in HUVECs, resulting in an increase in the expression of HO-1. Taking our data together, we can conclude that, in HUVECs, geraniol inhibits Ox-LDL-induced inflammation and oxidative stress by targeting PI3/AKT/NRF2. [ABSTRACT FROM AUTHOR]

Homologous chromosomes pair with each other during meiosis, culminating in the formation of the synaptonemal complex (SC), which is coupled with meiotic recombination. In this study, we showed that a meiosis-specific depletion mutant of a cullin (Cdc53) in the SCF (Skp-Cullin-F-box) ubiquitin ligase, which plays a critical role in cell cycle regulation during mitosis, is deficient in SC formation. However, the mutant is proficient in forming crossovers, indicating the uncoupling of meiotic recombination with SC formation in the mutant. Furthermore, the deletion of the PCH2 gene encoding a meiosis-specific AAA+ ATPase suppresses SC-assembly defects induced by CDC53 depletion. On the other hand, the pch2 cdc53 double mutant is defective in meiotic crossover formation, suggesting the assembly of SC with unrepaired DNA double-strand breaks. A temperature-sensitive mutant of CDC4 , which encodes an F-box protein of SCF, shows meiotic defects similar to those of the CDC53 -depletion mutant. These results suggest that SCF Cdc4 , probably SCF Cdc4 -dependent protein ubiquitylation, regulates and collaborates with Pch2 in SC assembly and meiotic recombination., (© 2020 Zhu et al.)