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Exposure to fine particulate matter (PM2.5) is correlated to atherosclerosis, but the mechanism remains largely undefined. Iron overload is a significant contributor to atherosclerosis, and iron homeostasis is highly regulated by the hepcidin-ferroportin (FPN) axis. Here we aimed to investigate the association between iron overload and PM2.5-induced atherosclerotic mice. Apolipoprotein E knockout (ApoE ) mice were randomly assigned to filtered air (FA group) or PM2.5 (PM2.5 group) for 3-month inhalation. Daily PM2.5 mass concentrations, serum levels of ferritin, iron, pro-atherosclerotic cytokines and lipid profiles, atherosclerotic lesion areas, hepcidin, FPN and iron depositions in atherosclerotic lesions, hepcidin, FPN mRNA and protein expressions in the aorta were detected, respectively. The daily average concentration of atmospheric PM2.5 was 68.2±21.8μg/m . Serum levels of ferritin, iron, VEGF, MCP-1, IL-6, TNF-α, TC and LDL-C, atherosclerotic lesion areas, hepcidin and iron depositions in atherosclerotic lesions, hepcidin mRNA and protein expressions in the PM2.5 group were observably higher than those in the FA group. Nevertheless, FPN deposition in atherosclerotic lesions, FPN mRNA and protein expressions in the aorta of the PM2.5 group were markedly lower than those of the FA group. PM2.5 inhalation could exacerbate the formation and development of atherosclerosis in ApoE mice, the potential mechanisms may be partly associated with iron overload via the hepcidin-FPN axis, as well as iron-triggered systemic inflammation and hyperlipidemia. PM2.5 inhalation could exacerbate the formation and development of atherosclerosis in ApoE-/- mice, the potential mechanisms may be partly associated with iron overload via the hepcidin-FPN axis, as well as iron-triggered systemic inflammation and hyperlipidemia. Epigenetic and genetic alterations are crucial events in the onset and progression of human cancers including colorectal cancer (CRC). This work aims to probe the relevance of lysine demethylase 5B (KDM5B) to the progression of CRC and the possible molecules involved. KDM5B expression in CRC tissues and cells was determined. The association between KDM5B and the prognosis of patients was analyzed. Gain- and loss-of function studies of KDM5B were performed in HT-29 and KDM5B cells to explore the impact of KDM5B on cell behaviors. Expression of CC chemokine ligand 14 (CCL14) in CRC tissues and cells and its correlation with KDM5B were analyzed. Altered expression of CCL14 was introduced in CRC cells, and a Wnt/β-catenin-specific antagonist KYA1797K was induced in cells as well. KDM5B was abundantly expressed while CCL14 was poorly expressed in CRC tissues and cells. High KDM5B expression was relevant to poor prognosis of patients. https://www.selleckchem.com/products/slf1081851-hydrochloride.html Downregulation of KDM5B suppressed proliferation and aggressiveness of HT-29 cells, and reduced the growth of xenograft tumors in mice, while upregulation of KDM5B in SW480 cells led to reverse results. KDM5B reduced CCL14 expression through demethylation modification of H3K4me3. Upregulation of CCL14 suppressed colony formation and invasiveness of CRC cells. KDM5B downregulated CCL14 to activate the Wnt/β-catenin. Inhibition of β-catenin by KYA1797K blocked the oncogenic roles of KDM5B in cells and in xenograft tumors. This study suggested that KDM5B suppresses CCL14 through demethylation modification of H3K4me3, leading to activation of the Wnt/β-catenin and the CRC progression. This study suggested that KDM5B suppresses CCL14 through demethylation modification of H3K4me3, leading to activation of the Wnt/β-catenin and the CRC progression. Secretory clusterin (sCLU) plays an important role in tumor development and cancer progression. However, the molecular mechanisms and physiological functions of sCLU in oral cancer is unclear. We examined the impact of sCLU-mediated autophagy in cell survival and apoptosis inhibition in oral cancer. Immunohistochemical analysis was performed to analyze protein expression in patient samples. Autophagy and mitophagy was studied by immunofluorescence microscopy and Western blot. The gain and loss of function was studied by overexpression of plasmid and siRNA approaches respectively. Cellular protection against nutrient starvation and therapeutic stress by sCLU was studied by cell viability, caspase assay and meta-analysis. The data from oral cancer patients showed that the expression levels of sCLU, ATG14, ULK1, and PARKIN increased in grade-wise manners. Interestingly, sCLU overexpression promoted autophagy through AMPK/Akt/mTOR signaling pathway leading to cell survival and protection from long exposure serum starvation induced-apoptosis. Additionally, sCLU was demonstrated to interact with ULK1 and inhibition of ULK1 activity by SBI206965 was found to abolish sCLU-induced autophagy indicating critical role of ULK1 in induction of autophagy. Furthermore, sCLU was observed to promote expression of mitophagy-associated proteins in serum starvation conditions to protect cells from nutrient deprivation. The meta-analysis elucidated that high CLU expression is associated with therapy resistance in cancer and we demonstrated that sCLU-mediated mitophagy was revealed to inhibit cell death by cisplatin. The present investigation has highlighted the probable implications of the clusterin-induced autophagy in cell survival and inhibition of apoptosis in oral cancer. The present investigation has highlighted the probable implications of the clusterin-induced autophagy in cell survival and inhibition of apoptosis in oral cancer. Hypertension (HTN) in pregnancy is a major cause of maternal, foetal and neonatal morbimortality in both developing and developed countries. Arterial stiffness is a predictor of cardiovascular events and can be assessed through augmentation index (AIx) and pulse wave velocity (PWV). This study was intended to analyse the arterial stiffness in three categories, hypertensive pregnant women vs. healthy women (both pregnant and non-pregnant). Between 2018 and 2019, 150 women were prospectively included into three homogenous groups, of equal sizes (N=50) pregnant women with HTN (group 1), pregnant women without HTN (group 2), and non-pregnant women (group 3). We assessed pregnant women 3 times (in all three trimesters) and six weeks postpartum, and the women from the control group once. Significant differences (p<0.001) of the hemodynamic and arterial stiffness parameters and of the heart rate (HR) (p=0.006) were observed between groups 1 and 2. Women with pregnancy-induced HTN had different values of arterial function parameters long time before the first signs of high blood pressure (BP) occurred.
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