Electron-Sponge Nature of Polyoxometalates for Next-Generation Electrocatalytic Water Splitting and Nonvolatile Neuromorphic Devices.

Designing next-generation molecular devices typically necessitates plentiful oxygen-bearing sites to facilitate multiple-electron transfers. However, the theoretical limits of existing materials for energy conversion and information storage devices make it inevitable to hunt for new competitors. Polyoxometalates (POMs), a unique class of metal-oxide clusters, have been investigated exponentially due to their structural diversity and tunable redox properties.

Autophagy inhibits high glucose induced cardiac microvascular endothelial cells apoptosis by mTOR signal pathway.

Cardiac microvascular endothelial cells (CMECs) dysfunction is an important pathophysiological event in the cardiovascular complications induced by diabetes. However, the underlying mechanism is not fully clarified. Autophagy is involved in programmed cell death.

Autophagy mediates the beneficial effect of hypoxic preconditioning on bone marrow mesenchymal stem cells for the therapy of myocardial infarction.

Background: Stem cell therapy has emerged as a promising therapeutic strategy for myocardial infarction (MI). However, the poor viability of transplanted stem cells hampers their therapeutic efficacy. Hypoxic preconditioning (HPC) can effectively promote the survival of stem cells.

Autophagy regulates the apoptosis of bone marrow-derived mesenchymal stem cells under hypoxic condition via AMP-activated protein kinase/mammalian target of rapamycin pathway.

Bone marrow-derived mesenchymal stem cells (BM-MSCs) have been demonstrated as an ideal autologous stem cells source for cell-based therapy for myocardial infarction (MI). However, poor viability of donor stem cells after transplantation limits their therapeutic efficiency, whereas the underlying mechanism is still poorly understood. Autophagy, a highly conserved process of cellular degradation, is required for maintaining homeostasis and normal function.

Impact of losartan and angiotensin II on the expression of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 in rat vascular smooth muscle cells.

The present study aimed to investigate the impact of losartan and angiotensin II (AngII) on the expression of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1), secreted by rat vascular smooth muscle cells (VSMCs). Rat VSMCs were isolated and cultured in different concentrations of AngII and losartan for 24 h and western blot analysis and quantitative polymerase chain reaction were performed to observe the subsequent impact on the gene and protein expression of MMP-9 and TIMP-1. AngII was shown to promote the protein and gene expression of MMP-9 in VSMCs in a concentration-dependent manner.

Cyclosporin A suppresses proliferation of endothelial progenitor cells: involvement of nitric oxide synthase inhibition.

Objective: To investigate the effects of the potent immunosuppressive agent cyclosporin A (CsA) on the proliferation of human endothelial progenitor cells (EPCs) and endothelial nitric oxide synthase (eNOS) expression in EPCs.

Methods And Results: The EPCs were obtained from cultured mononuclear cells, which were isolated from the peripheral blood of healthy adults, and stimulated with CsA (10 microg/mL) in the presence or absence of either vascular endothelial growth factor (VEGF; 50 ng/mL) or L-arginine (1 mM). To explore the effect of different concentrations of CsA alone on EPC proliferation, some cells were treated with CsA in a series of final concentrations ranging from 0 to 10 microg/mL.