Volatile cinnamaldehyde induces systemic salt tolerance in the roots of rice (Oryza sativa).

Cinnamaldehyde (CA) is a volatile plant secondary metabolite that exhibits strong anti-pathogenic activities. Nonetheless, less is known about the effect of CA on plant tolerance to abiotic stresses. In this study, we delineated the effects of CA fumigation on rice roots (Oryza Sativa L cv. TNG67) under salinity stress (200 mM NaCl). Our result showed that CA vapor significantly alleviated salinity-induced ROS accumulation and cell death. This CA-induced alleviation appears to be mediated primarily by the upregulation of proline metabolism genes, the rapid proline accumulation, and the decrease of Na+ /K+ ratio as early as 3 h after NaCl treatment. Of note, the activities of peroxidase (POD; EC 1.11.1.7) isozymes a and b were decreased by CA fumigation, and the activities of catalase (CAT; EC 1.11.1.6) and superoxide dismutase (SOD; EC 1.15.1.1) were not significantly affected. Our findings suggest that CA vapor might be useful for priming rice roots to withstand salinity stress, which is more prevalent due to the ongoing global climate change. To the best of our knowledge, this is the first study to show modulation of macro- and micro-elements as well as antioxidative factors after CA fumigation of salinity-stressed rice roots.

Sleep Deprivation Promotes Endothelial Inflammation and Atherogenesis by Reducing Exosomal miR-182-5p.

BACKGROUND: Insufficient or disrupted sleep increases the risk of cardiovascular disease, including atherosclerosis. However, we know little about the molecular mechanisms by which sleep modulates atherogenesis. This study aimed to explore the potential role of circulating exosomes in endothelial inflammation and atherogenesis under sleep deprivation status and the molecular mechanisms involved. METHODS: Circulating exosomes were isolated from the plasma of volunteers with or without sleep deprivation and mice subjected to 12-week sleep deprivation or control littermates. miRNA array was performed to determine changes in miRNA expression in circulating exosomes. RESULTS: Although the total circulating exosome levels did not change significantly, the isolated plasma exosomes from sleep-deprived mice or human were a potent inducer of endothelial inflammation and atherogenesis. Through profiling and functional analysis of the global microRNA in the exosomes, we found miR-182-5p is a key exosomal cargo that mediates the proinflammatory effects of exosomes by upregulation of MYD88 (myeloid differentiation factor 88) and activation of NF-ĸB (nuclear factor kappa-B)/NLRP3 pathway in endothelial cells. Moreover, sleep deprivation or the reduction of melatonin directly decreased the synthesis of miR-182-5p and led to the accumulation of reactive oxygen species in small intestinal epithelium. CONCLUSIONS: The findings illustrate an important role for circulating exosomes in distant communications, suggesting a new mechanism underlying the link between sleep disorder and cardiovascular disease.

One night of sleep deprivation induces release of small extracellular vesicles into circulation and promotes platelet activation by small EVs.

Extracellular vesicles (EVs) are emerging as key players in intercellular communication. Few studies have focused on EV levels in subjects with sleep disorders. Here, we aimed to explore the role of acute sleep deprivation on the quantity and functionality of circulating EVs, and their tissue distribution. EVs were isolated by ultracentrifugation from the plasma of volunteers and animals undergoing one night of sleep deprivation. Arterio-venous shunt, FeCl3 thrombus test and thrombin-induced platelet aggregation assay were conducted to evaluate the in vivo and in vitro bioactivity of small EVs. Western blotting was performed to measure the expression of EV proteins. The fate and distribution of circulating small EVs were determined by intravital imaging. We found that one night of sleep deprivation triggers release of small EVs into the circulation in both healthy individuals and animals. Injection of sleep deprivation-liberated small EVs into animals increased thrombus formation and weight in thrombosis models. Also, sleep deprivation-liberated small EVs promoted platelet aggregation induced by thrombin. Mechanistically, sleep deprivation increased the levels of HMGB1 protein in small EVs, which play important roles in platelet activation. Furthermore, we found sleep deprivation-liberated small EVs are more readily localize in the liver. These data suggested that one night of sleep deprivation is a stress for small EV release, and small EVs released here may increase the risk of thrombosis. Further, small EVs may be implicated in long distance signalling during sleep deprivation-mediated adaptation processes.