The same effect was also found in primary dermal fibroblasts from AhR−/− mice, further supporting that AhR is involved in cholesterol maintenance.
Examples of pathways with more than one represented gene include the renin-angiotensinogen pathway with three genes (ACE, AGTR1, EGF), and the cholesterol maintenance pathway with four genes in the assay (APOB, CETP, LDLR, LPL, and FABP2).
Endocytosis in eukaryotes is important for uptake of nutrients (e.g. iron, and cholesterol esters), maintenance of cell volume, and for modulation of cell signaling (reviewed in [1]).
The anti-atherogenic properties of HDL cholesterol (including maintenance of endothelial function [nitric oxide], reverse cholesterol transport, and anti-inflammatory properties) might protect against arterial stiffening.
Generally, the liver is considered to be the primary organ responsible for cholesterol homeostasis maintenance, by regulating cholesterol synthesis and uptake as well as cholesterol excretion into bile acids [ 37].
We also observed an up-regulation of KHK (ketohexokinase or fructokinase), which initiates the intracellular catabolism of a large proportion of dietary carbohydrates, as well as an up-regulation of STARD5, a cholesterol-binding protein that does not have well-understood functions but is thought to be important for cholesterol metabolism and maintenance of cellular homeostasis[32].
However, blood pressure control, total cholesterol control and maintenance of renal function (measured by ACR) largely remained unchanged over the study period.
While it is possible to reduce the volume of ER+ tumors by inhibiting the production of estrogen it is important to consider that estrogen plays an integral role in the normal physiology of women by controlling diverse processes such as cholesterol production and maintenance of bone density [ 6].
Here we demonstrate that cellular sterol depletion suppresses, and sterol loading induces, alternative splicing of multiple genes involved in the maintenance of cholesterol homeostasis including HMGCR and LDLR, the key regulators of cellular cholesterol biosynthesis and uptake, respectively.
The maintenance of cholesterol levels is essential for functional caveolae and depends, in part, on the interaction of cholesterol with caveolin-1 (Cav-1), the major structural component of caveolae [ 7].
The LDL receptor is the key component in the maintenance of cholesterol homeostasis in the body, playing a pivotal role by regulating the hepatic catabolism of LDL cholesterol.
