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Changes in Sertoli Cell Structure and Function
Published in Tom O. Abney, Brooks A. Keel, The Cryptorchid Testis, 2020
David M. de Kretser, Gail P. Risbridger
Subsequently increased vacuolization of Sertoli cells was noted which consisted of two types; the first type resulted from the dilatation of cisternae of smooth endoplasmic reticulum whereas the second specifically involves a dilation of the intercellular space at the sites of the inter-Sertoli cell junctions (see Figure 1). Despite these changes in the inter-Sertoli cell junctional complexes, the function of the blood-testis barrier appeared to be intact.17 It seems likely that the increased lipid in Sertoli cells is not the result of phagocytosis of degenerating germ cells since, when tests without germ cells are made cryptorchid, a similar lipid accumulation occurs.18 Analysis of the lipid showed an increase in cholesterol and cholesterol esters.19
Atherosclerosis
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Cholesterol and cholesteryl esters accumulate in greatest amount at all stages of the evolution of atherosclerotic lesions.73,107,595,596 Accumulation of cholesterol can cause occlusion of the lumen of the affected blood vessels (Plate 4). The principal source of cholesterol is the blood plasma and the presence of the protein portion from plasma lipoproteins in the arterial lesions suggests that the cholesterol crosses the endothelial barrier in the form of lipoproteins. Lipoproteins can go from the vessel lumen into the lining endothelial cells by a passive transport process and are transported through the endothelial cell into the intima by either passive or active mechanisms. Lipids go through or are exchanged independently of the protein moiety. However, feeding experiments with labeled cholesterol have shown that it is incorporated into plasma lipoproteins and that it also appears in the aorta.
The Stimulation of Steroid Biosynthesis by Luteinizing Hormone
Published in Mario Ascoli, Luteinizing Hormone Action and Receptors, 2019
Anita H. Payne, Patrick G. Quinn, John R. D. Stalvey
Intracellular cholesterol can be stored as cholesteryl esters in lipid droplets. The extent of cholesterol storage in gonads varies among different cell types in the same species. In a steroid hormone-producing cell, the amount of cholesterol stored as cholesteryl esters is dependent on the intracellular concentration of free cholesterol, which in turn is determined by the availability of exogenous cholesterol, by the endogenous synthesis of cholesterol, and by the rate of steroid hormone producton. There are two enzymes that are directly related to the amount of cholesterol stored as cholesteryl esters: acyl-coenzyme A:cholesterol acyltransferase (ACAT) and cholesteryl esterase (cholesteryl ester hydrolase). ACAT is associated with the smooth endoplasmic reticulum and catalyzes the esterification of free cholesterol; cholesteryl esterase catalyzes the hydrolysis of cholesteryl esters and is found predominantly in the cytosol.
Human ovarian granulosa cells use clathrin-mediated endocytosis for LDL uptake: immunocytochemical and electron microscopic study
Published in Ultrastructural Pathology, 2023
Aynur Abdulova, Merjem Purelku, Hakan Sahin, Gamze Tanrıverdi
Steroidogenesis is a complex process between multiple enzymes and substrates by which cholesterol is converted into steroid hormones. Cholesterol is stored in lipid droplets (LDs) as cholesterol esters (CEs) within the steroidogenic tissue. The cholesterol that is required for steroidogenesis which is being initiated in response to a hormonal stimulus is provided by the mobilization of these stored CEs within the cells.3 There are two different forms of cholesterol which are known as high-density lipoprotein (HDL) and low-density lipoprotein (LDL). Studies are focused on the fact that granulosa cells use the LDL-receptor (LDLR)-mediated endocytic pathway for steroid biosynthesis. LDLR is an important protein that functions to mediate the uptake of LDL cholesterol, which is a specific substrate for steroid hormone production.3–5 Many different endocytic pathways have been described in eukaryotic cells, but the main pathway for LDL transport has been reported to be the clathrin-mediated endocytosis pathway.6,7 However, no study that clarifies LDL internalization in human granulosa cells and whether the clathrin-mediated endocytic pathway is functional in this process has yet been published.
Pharmacology, toxicity and pharmacokinetics of acetylshikonin: a review
Published in Pharmaceutical Biology, 2020
Zhiqin Zhang, Jie Bai, Yawen Zeng, Mengru Cai, Yu Yao, Huimin Wu, Longtai You, Xiaoxv Dong, Jian Ni
Acyl-CoA: cholesterol acyltransferase (ACAT) is responsible for the intracellular esterification of free cholesterol with fatty acyl-CoA to produce cholesterol esters (Chang et al. 2006). An et al. (2007) demonstrated that acetylshikonin was found to weakly suppress human ACAT-1 and ACAT-2, but its analogue propanoylshikonin exerted strong inhibitory effect on ACAT, indicating that the inhibitory potency was associated with the length of the acyl group. In 3T3-L1 cells, acetylshikonin suppressed adipocyte differentiation and the expression of adipogenic transcription factors (PPARγ and C/EBPα) (Gwon et al. 2012). Furthermore, treatment of high fat diet (HFD)-induced obese rats with acetylshikonin led to reductions in body weight, white adipose tissue content, serum triglycerides, and free fatty acid levels. The lipid-regulatory effect was attributed to triacylglycerol hydrolysis via regulation of protein kinase A (PKA) signalling in 3T3-L1 cells (Su et al. 2016a). Acetylshikonin had an excellent therapeutic effect on obesity and non-alcoholic fatty liver disease in spontaneous obese db/db mice. The mechanisms were involved in marked suppression of alanine aminotransferase, aspartate aminotransferase, and pro-inflammatory cytokines (TNF-α, IL-6 and IL-1β), as well as downregulation of sterol regulatory element-bindingprotein-1 (SREBP-1), fatty acid synthetase (FAS), and 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) (Su et al. 2016b).
Platelet-lymphocyte ratio (PLR) and all-cause mortality in general population: insights from national health and nutrition education survey
Published in Platelets, 2019
Kanupriya Mathur, Nargiza Kurbanova, Rehan Qayyum
Platelet and lymphocyte counts were reported in 1000 cells/µL. PLR was calculated by dividing the platelet count by the lymphocyte count. The hazard ratio with 95% confidence intervals (CIs) were reported for difference from the lowest PLR quartile. Serum creatinine was measured using the Jaffe rate method (kinetic alkaline picrate) and glomerular filtration rate (GFR) was calculated using Chronic Kidney Disease Epidemiology Collaboration equation and was reported in ml/min/1.73 m2. Total cholesterol was measured enzymatically in serum or plasma in a series of coupled reactions that hydrolyze cholesteryl esters. Serum c-reactive protein (CRP) was quantified using latex-enhanced nephelometry. Serum glucose level was measured using the Beckman Synchron LX20 test (Beckman Coulter, Fullerton, CA, USA) on refrigerated specimens. Diabetes was defined as random glucose >200 mg/dL, HbA1c >7%, self-report of diabetes diagnosis, or taking diabetes medications.