ER stress upregulated PGE₂/IFNγ-induced IL-6 expression and down-regulated iNOS expression in glial cells.

The disruption of endoplasmic reticulum (ER) function can lead to neurodegenerative disorders, in which inflammation has also been implicated. We investigated the possible correlation between ER stress and immune function using glial cells. We demonstrated that ER stress synergistically enhanced prostaglandin (PG) E₂ + interferon (IFN) γ-induced interleukin (IL)-6 production.

ER stress-mediated regulation of immune function under glucose-deprived condition in glial cells: up- and down-regulation of PGE2 + IFNγ-induced IL-6 and iNOS expressions.

Glucose metabolism plays central role in maintaining brain function. Under ischemic condition, where glucose levels were reduced, glial cells induce pro-inflammatory cytokine production. In the present study, we found prostaglandin (PG) E2+interferon (IFN) γ-induced interleukin (IL)-6 production was enhanced under glucose-deprived condition in the primary cultured glial cells.

Excitonic coupling in linear and trefoil trimer perylenediimide molecules probed by single-molecule spectroscopy.

Perylenediimide (PDI) molecules are promising building blocks for photophysical studies of electronic interactions within multichromophore arrays. Such PDI arrays are important materials for fabrication of molecular nanodevices such as organic light-emitting diodes, organic semiconductors, and biosensors because of their high photostability, chemical and physical inertness, electron affinity, and high tinctorial strength over the entire visible spectrum. In this work, PDIs have been organized into linear (L3) and trefoil (T3) trimer molecules and investigated by single-molecule fluorescence microscopy to probe the relationship between molecular structures and interchromophoric electronic interactions.

Relaxation in Thin Polymer Films Mapped across the Film Thickness by Astigmatic Single-Molecule Imaging.

We have studied relaxation processes in thin supported films of poly(methyl acrylate) at the temperature corresponding to 13 K above the glass transition by monitoring the reorientation of single perylenediimide molecules doped into the films. The axial position of the dye molecules across the thickness of the film was determined with a resolution of 12 nm by analyzing astigmatic fluorescence images. The average relaxation times of the rotating molecules do not depend on the overall thickness of the film between 20 and 110 nm.

Methylglyoxal has deleterious effects on thioredoxin in human aortic endothelial cells.

Methylglyoxal (MG), a precursor of advanced glycation end products (AGEs), is elevated in diabetic patient's plasma. Some studies have demonstrated that MG induces oxidative stress and apoptosis. Thioredoxin (Trx) is a cytoprotective protein with anti-oxidative and anti-apoptosis functions.

Multi-beam single-molecule defocused fluorescence imaging reveals local anisotropic nature of polymer thin films.

We developed a method to determine full three-dimensional orientation distribution of individual molecules based on wide-field defocused fluorescence imaging. Excitation efficiencies of out-of-plane oriented molecules were improved dramatically by illuminating molecules with multiple laser beams. Our high throughput approach allowed us to obtain unbiased statistical distributions of orientations of doped molecules in spin-coated polymer thin films.

Buthionine sulfoximine promotes methylglyoxal-induced apoptotic cell death and oxidative stress in endothelial cells.

Methylglyoxal (MG), a reactive dicarbonyl produced during glucose metabolism, is found at high levels in the blood of diabetic patients. MG induces oxidative stress and apoptosis. There is evidence that MG causes glutathione (GSH) depletion.

A unique modulator of endoplasmic reticulum stress-signalling pathways: the novel pharmacological properties of amiloride in glial cells.

Background And Purpose: Stress on the endoplasmic reticulum (ER) can trigger rescuer responses such as the unfolded protein response (UPR). However, pharmacological modulators of these ER-regulated stress responses are not well understood. In the present study, we found that amiloride, a potassium-sparing diuretic, has unique properties relating to such stress.

Methylglyoxal causes dysfunction of thioredoxin and thioredoxin reductase in endothelial cells.

Methylglyoxal (MG), a reactive dicarbonyl produced during glucose metabolism, induces oxidative stress and apoptosis. Under hyperglycemic conditions, the abnormal accumulation of MG is related to the development of diabetic complications. We examined the effects of MG on thioredoxin (Trx) and glutaredoxin (Grx) systems, two thiol-disulfide oxidoreductase systems that protect against oxidative damage of proteins, in bovine aortic endothelial cells (BAECs).

[methylglyoxal-induced superoxide anion production in endothelial cells].

Methylglyoxal (MG), a highly reactive dicarbonyl compound, is a metabolic by-product of glycolysis. MG is often detected at high levels in the blood of diabetic patients. We examined whether MG was capable of inducing reactive oxygen species (ROS) production in bovine aortic endothelial cells (BAECs).

Multidrug-resistance-associated protein plays a protective role in menadione-induced oxidative stress in endothelial cells.

Aims: Menadione, a redox-cycling quinone known to cause oxidative stress, binds to reduced glutathione (GSH) to form glutathione S-conjugate. Glutathione S-conjugates efflux is often mediated by multidrug-resistance-associated protein (MRP). We investigated the effect of a transporter inhibitor, MK571 (3-[[3-[2-(7-chloroquinolin-2-yl)vinyl]phenyl]-(2-dimethylcarbamoylethylsulfanyl)methylsulfanyl] propionic acid), on menadione-induced oxidative stress in bovine aortic endothelial cells (BAECs).