scholarly journals Extracellular-Nitric Oxide-Mediated Platelet-cGMP Production in Type 2 Diabetics Correlates Inversely with Plasma Membrane Cholesterol Levels

2009 ◽  
pp. 267-273
Author(s):  
Shane Miersch ◽  
Inga Sliskovic ◽  
Arianna Vignini ◽  
Laura Mazzanti ◽  
Bulent Mutus
Keyword(s):  
Nitric Oxide ◽  
Plasma Membrane ◽  
Membrane Cholesterol ◽  
Cgmp Production ◽  
Cholesterol Levels ◽  
Type 2 Diabetics ◽  
Plasma Membrane Cholesterol

scholarly journals Distribution of membrane cholesterol of adrenal cortical cells after corticotropin stimulation

1983 ◽  
Vol 214 (2) ◽  
pp. 561-567 ◽  
Author(s):  
O M Conneely ◽  
J M Greene ◽  
D R Headon ◽  
J Hsiao ◽  
F Ungar
Keyword(s):  
Plasma Membrane ◽  
Cholesteryl Ester ◽  
Membrane Cholesterol ◽  
Cortical Cells ◽  
Cholesterol Levels ◽  
Adrenal Cortical Cells ◽  
Hydrolysis Of ◽  
Plasma Membrane Cholesterol ◽  
Corticotropin Stimulation ◽  
Stimulation Of

Membrane cholesterol in adrenal cortical cells is enriched in the plasma membrane. Stimulation of isolated adrenal cortical cells with corticotropin leads to the production of corticosterone. At high levels of corticotropin, cholesterol for corticosterone synthesis arises by hydrolysis of cellular cholesteryl ester, whereas at lower levels of corticotropin cholesteryl ester levels are unchanged from control values and there is a decrease in plasma-membrane cholesterol levels.

scholarly journals Elevated Basal Insulin Secretion in Type 2 Diabetes Caused by Reduced Plasma Membrane Cholesterol

2016 ◽  
Vol 30 (10) ◽  
pp. 1059-1069 ◽  
Author(s):  
Vini Nagaraj ◽  
Abdulla S. Kazim ◽  
Johan Helgeson ◽  
Clemens Lewold ◽  
Satadal Barik ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Plasma Membrane ◽  
Insulin Secretion ◽  
Basal Insulin ◽  
Membrane Cholesterol ◽  
Basal Insulin Secretion ◽  
Plasma Membrane Cholesterol

scholarly journals Plasma Membrane Cholesterol Content Affects Nitric Oxide Diffusion Dynamics and Signaling

2008 ◽  
Vol 283 (27) ◽  
pp. 18513-18521 ◽  
Author(s):  
Shane Miersch ◽  
Michael Graham Espey ◽  
Ruchi Chaube ◽  
Arzu Akarca ◽  
Rodney Tweten ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Plasma Membrane ◽  
Cholesterol Content ◽  
Membrane Cholesterol ◽  
Diffusion Dynamics ◽  
Nitric Oxide Diffusion ◽  
Plasma Membrane Cholesterol

scholarly journals Shear stress activates mitochondrial oxidative phosphorylation by reducing plasma membrane cholesterol in vascular endothelial cells

2020 ◽  
Vol 117 (52) ◽  
pp. 33660-33667
Author(s):  
Kimiko Yamamoto ◽  
Yoshitsugu Nogimori ◽  
Hiromi Imamura ◽  
Joji Ando
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Plasma Membrane ◽  
Vascular Endothelial Cells ◽  
Membrane Cholesterol ◽  
Vascular Endothelial ◽  
Mitochondrial Oxidative Phosphorylation ◽  
Atp Production ◽  
Cholesterol Levels ◽  
Plasma Membrane Cholesterol

Vascular endothelial cells (ECs) sense and respond to hemodynamic shear stress, which is critical for circulatory homeostasis and the pathophysiology of vascular diseases. The mechanisms of shear stress mechanotransduction, however, remain elusive. We previously demonstrated a direct role of mitochondria in the purinergic signaling of shear stress: shear stress increases mitochondrial adenosine triphosphate (ATP) production, triggering ATP release and Ca2+ signaling via EC purinoceptors. Here, we showed that shear stress rapidly decreases cholesterol in the plasma membrane, thereby activating mitochondrial ATP production. Imaging using domain 4 mutant-derived cholesterol biosensors showed that the application of shear stress to cultured ECs markedly decreased cholesterol levels in both the outer and inner plasma membrane bilayers. Flow cytometry showed that the cholesterol levels in the outer bilayer decreased rapidly after the onset of shear stress, reached a minimum (around 60% of the control level) at 10 min, and plateaued thereafter. After the shear stress ceased, the decreased cholesterol levels returned to those seen in the control. A biochemical analysis showed that shear stress caused both the efflux and the internalization of plasma membrane cholesterol. ATP biosensor imaging demonstrated that shear stress significantly increased mitochondrial ATP production. Similarly, the treatment of cells with methyl-β-cyclodextrin (MβCD), a membrane cholesterol-depleting agent, increased mitochondrial ATP production. The addition of cholesterol to cells inhibited the increasing effects of both shear stress and MβCD on mitochondrial ATP production in a dose-dependent manner. These findings indicate that plasma membrane cholesterol dynamics are closely coupled to mitochondrial oxidative phosphorylation in ECs.

scholarly journals Monoclonal antibody detection of plasma membrane cholesterol microdomains responsive to cholesterol trafficking

2001 ◽  
Vol 42 (9) ◽  
pp. 1492-1500 ◽  
Author(s):  
Howard S. Kruth ◽  
Ina Ifrim ◽  
Janet Chang ◽  
Lia Addadi ◽  
Daniele Perl-Treves ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Plasma Membrane ◽  
Antibody Detection ◽  
Membrane Cholesterol ◽  
Cholesterol Trafficking ◽  
Plasma Membrane Cholesterol

scholarly journals Three pools of plasma membrane cholesterol and their relation to cholesterol homeostasis

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Akash Das ◽  
Michael S Brown ◽  
Donald D Anderson ◽  
Joseph L Goldstein ◽  
Arun Radhakrishnan
Keyword(s):  
Plasma Membrane ◽  
Regulatory Mechanism ◽  
Low Density Lipoprotein ◽  
Human Fibroblasts ◽  
Density Lipoprotein ◽  
Cholesterol Homeostasis ◽  
Mutant Form ◽  
Perfringolysin O ◽  
Cholesterol Levels ◽  
Plasma Membrane Cholesterol

When human fibroblasts take up plasma low density lipoprotein (LDL), its cholesterol is liberated in lysosomes and eventually reaches the endoplasmic reticulum (ER) where it inhibits cholesterol synthesis by blocking activation of SREBPs. This feedback protects against cholesterol overaccumulation in the plasma membrane (PM). But how does ER know whether PM is saturated with cholesterol? In this study, we define three pools of PM cholesterol: (1) a pool accessible to bind 125I-PFO*, a mutant form of bacterial Perfringolysin O, which binds cholesterol in membranes; (2) a sphingomyelin(SM)-sequestered pool that binds 125I-PFO* only after SM is destroyed by sphingomyelinase; and (3) a residual pool that does not bind 125I-PFO* even after sphingomyelinase treatment. When LDL-derived cholesterol leaves lysosomes, it expands PM's PFO-accessible pool and, after a short lag, it also increases the ER's PFO-accessible regulatory pool. This regulatory mechanism allows cells to ensure optimal cholesterol levels in PM while avoiding cholesterol overaccumulation.

Cell culturing in a three-dimensional matrix affects the localization and properties of plasma membrane cholesterol

2009 ◽  
Vol 33 (10) ◽  
pp. 1079-1086 ◽  
Author(s):  
Nadezhda Stefanova ◽  
Galya Staneva ◽  
Diana Petkova ◽  
Teodora Lupanova ◽  
Roumen Pankov ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Three Dimensional ◽  
Membrane Cholesterol ◽  
Dimensional Matrix ◽  
Cell Culturing ◽  
Plasma Membrane Cholesterol
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