Hydrogen Repairs LPS-Induced Endothelial Progenitor Cells Injury via PI3K/AKT/eNOS Pathway.

Endotoxins and other harmful substances may cause an increase in permeability in endothelial cells (ECs) monolayers, as well as ECs shrinkage and death to induce lung damage. Lipopolysaccharide (LPS) can impair endothelial progenitor cells (EPCs) functions, including proliferation, migration, and tube formation. EPCs can migrate to the damaged area, differentiate into ECs, and participate in vascular repair, which improves pulmonary capillary endothelial dysfunction and maintains the integrity of the endothelial barrier. Hydrogen (H2) contributes to the repairment of lung injury and the damage of ECs. We therefore speculate that H2 protects the EPCs against LPS-induced damage, and it's mechanism will be explored. The bone marrow-derived EPCs from ICR Mice were treated with LPS to establish a damaged model. Then EPCs were incubated with H2, and treated with PI3K inhibitor LY294002 and endothelial nitric oxide synthase (eNOS) inhibitor L-NAME. MTT assay, transwell assay and tube formation assay were used to detect the proliferation, migration and angiogenesis of EPCs. The expression levels of target proteins were detected by Western blot. Results found that H2 repaired EPCs proliferation, migration and tube formation functions damaged by LPS. LY294002 and L-NAME significantly inhibited the repaired effect of H2 on LPS-induced dysfunctions of EPCs. H2 also restored levels of phosphor-AKT (p-AKT), eNOS and phosphor-eNOS (p-eNOS) suppressed by LPS. LY294002 significantly inhibited the increase of p-AKT and eNOS and p-eNOS expression exposed by H2. L-NAME significantly inhibited the increase of eNOS and p-eNOS expression induced by H2. H2 repairs the dysfunctions of EPCs induced by LPS, which is mediated by PI3K/AKT/eNOS signaling pathway.

HDL and microRNAs.

In previous chapters, we know that high-density lipoproteins (HDLs) could act at multiple cell lines and then trigger intracellular molecular pathway to prevent several metabolic diseases. Besides the classic genes regulating cholesterol efflux and reverse cholesterol transport (RCT), microRNAs (miRNAs) could also affect HDLs biogenesis, metabolism, and functions. This chapter summarizes the miRNAs, which regulate HDLs functions in table. In addition, HDLs are good vectors for miRNAs. They could carry miRNAs in circulation and take them into several cells such as macrophages and endothelial cells. Complete understanding of the miRNAs associated with HDL regulation would give us broader insights to prevent and treat metabolic diseases.

Comparison of Biochemical Parameters between Mouse Model and Human after Paraquat Poisoning.

BACKGROUND: This study was designed to investigate differences in biochemical parameters between mouse and humans after paraquat (PQ) poisoning and develop a suitable animal model for studying organ damage after PQ poisoning. The prognostic factors of PQ-poisoned patients were further analyzed. METHODS: Thirty C57BL/6J mice were randomly divided into five groups (control, sham, and 3 PQ doses), and the mouse model was established by intragastric administration of PQ. Physiological indexes such as the body weight, mental state, and mortality rate were observed. Biochemical parameters were analyzed 24 h after PQ poisoning. We also performed a retrospective analysis of clinical data from 29 patients with PQ poisoning admitted to the Emergency Department of the Affiliated Hospital of Taishan Medical College between April 2016 and February 2018. Biochemical parameters were compared between the mouse model and patients with PQ poisoning. RESULTS: In the PQ poisoning mouse model, the lethal dose group PQ360 showed remarkable increases in serum levels of potassium (K+), carbon dioxide (CO2), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) compared with the nonlethal dose PQ100 and PQ200 groups. The biochemical results of the patients showed that K+ and Cl- levels were significantly reduced in the death group compared to the survival group. Levels of ALT, AST, blood urea nitrogen (BUN), and amylase were higher, and the neutrophil-to-lymphocyte ratio (NLR) was increased in the death group compared with the survival group. CONCLUSIONS: The combination of age, PQ dosage, K+, Cl-, BUN, ALT, AST, amylase, and NLR can be used to more accurately predict the outcome of patients with PQ poisoning. C57 mice are an appropriate animal model to study liver and kidney functions following PQ exposure.

Salvinia-like slippery surface with stable and mobile water/air contact line.

Superhydrophobic surfaces are widely used in many industrial settings, and mainly consist of rough solid protrusions that entrap air to minimize the liquid/solid area. The stability of the superhydrophobic state favors relatively small spacing between protrusions. However, this in turn increases the lateral adhesion force that retards the mobility of drops. Here we propose a novel approach that optimizes both properties simultaneously. Inspired by the hydrophobic leaves of Salvinia molesta and the slippery Nepenthes pitcher plants, we designed a Salvinia-like slippery surface (SSS) consisting of protrusions with slippery heads. We demonstrate that compared to a control surface, the SSS exhibits increased stability against pressure and impact, and enhanced lateral mobility of water drops as well as reduced hydrodynamic drag. We also systematically investigate the wetting dynamics on the SSS. With its easy fabrication and enhanced performance, we envision that SSS will be useful in a variety of fields in industry.

Advances of Endothelial Progenitor Cells in the Development of Depression.

Depression is a major psychological disease of human beings. With the severity of depression, it elevates the risk of cardiovascular disease (CVD), especially acute coronary syndrome (ACS), resulting in serious harm to human health. The number of endothelial progenitor cells (EPCs) is closely related to the development of depression. It has been reported that the number of peripheral blood EPCs in patients with depression was reduced. However, effects on the function of EPCs in depression are still unclear. This paper aims to analyze and summarize the research of EPCs in depression, and we envision that EPCs might act as a new target for evaluating the severity of depression and its complications.

Circulating endothelial progenitor cells from septic patients are associated with different infectious organisms.

BACKGROUND: In sepsis, endothelial progenitor cells (EPCs) play a central role in the repair of endothelial injury by enhancing the processes of re-endothelialization and angiogenesis. However, the surface markers of EPCs have yet to be standardized, and Changes of EPCs in quantities and functions with different infectious organisms are still unclear. This study explored the relationship between the percentages of EPCs and various infectious organisms in patients with sepsis. METHODS: Thirty-nine septic patients and 20 healthy controls were enrolled in this study. The percentages of CD34+/KDR+, CD133+/KDR+, CD34+/CD133+/KDR+, CD34+, CD133+, and KDR+ cells in different groups of septic patients and the healthy controls were analyzed by flow cytometry. RESULTS: The peripheral blood of septic patients had higher percentages of EPCs than that of the healthy controls. There were no significant differences in the percentages of EPCs between the sepsis and septic shock groups, nor between the survival group and the non-survival group. Additionally, the percentages of CD34+/CD133+/KDR+ cells in the gram-positive bacteremia group were significantly higher than those in the gram-negative bacteremia group and the negative blood culture group. The percentage of KDR+ cells in both the gram-positive bacteremia group and the gram-negative bacteremia group was significantly higher than that in the negative blood culture group. CONCLUSIONS: The percentages of circulating EPCs in patients with sepsis are associated with different infectious organisms.

An ApoA-I Mimic Peptide of 4F Promotes SDF-1α Expression in Endothelial Cells Through PI3K/Akt/ERK/HIF-1α Signaling Pathway.

Atherosclerosis (AS) seriously impairs the health of human beings and is manifested initially as endothelial cells (ECs) impairment and dysfunction in vascular intima, which can be alleviated through mobilization of endothelial progenitor cells (EPCs) induced by stromal-cell-derived factor-1α (SDF-1α). A strong inverse correlation between HDL and AS has been proposed. The aim of the present work is to investigate whether 4F, an apolipoprotein A-I (apoA-I, major component protein of HDL) mimic peptide, can upregulate SDF-1α in mice and human umbilical vein endothelial cells (HUVECs) and the underlying mechanism. The protein levels of SDF-1α were measured by ELISA assay. Protein levels of HIF-1α, phosphorylated Akt (p-Akt), and phosphorylated ERK (p-ERK) were evaluated by Western blotting analysis. The results show that L-4F significantly upregulates protein levels of HIF-1α, Akt, and ERK, which can be inhibited by the PI3K inhibitor, LY294002, or ERK inhibitor, PD98059, respectively. Particularly, LY294002 can downregulate the levels of p-ERK, while PD98059 cannot suppress that of p-Akt. D-4F can upregulate the levels of HIF, p-Akt, and p-ERK in the abdominal aorta and inferior vena cava from mice. These results suggest that 4F promotes SDF-1α expression in ECs through PI3K/Akt/ERK/HIF-1α signaling pathway.