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Endocrine and Metabolic Side Effects
Published in Ayse Serap Karadag, Berna Aksoy, Lawrence Charles Parish, Retinoids in Dermatology, 2019
Ayse Serap Karadag, Emin Ozlu, Bodo C. Melnik
ATP-binding cassette subfamily A, member 1 (ABCA1) is a membrane transporter responsible for cholesterol efflux and plays a pivotal role in regulating cellular cholesterol levels. ABCA1 is expressed in keratinocytes, where it is negatively regulated by a decrease in cellular cholesterol levels or altered permeability barrier requirements and positively regulated by activators of LXR, PPARs, and RXR or increases in cellular cholesterol levels (173). In an animal model of Alzheimer disease, the RXR agonist of bexarotene induced the expression of ABCA1 and promoted cellular cholesterol efflux (174).
Lipoprotein Metabolism and Implications for Atherosclerosis Risk Determination and Treatment Decisions
Published in P. K. Shah, Risk Factors in Coronary Artery Disease, 2006
H. Robert Superko, Szilard Voros, Spencer King III
Cholesterol efflux from cells is regulated in part by the ABC1 transporter (195). It serves to efflux cholesterol from an intracellular location to lipid-poor apo A-I and forms nascent HDL particles, which can then be converted into mature HDL particles by the action of LCAT. The important role of ABC1 in lipoprotein metabolism and atherosclerosis was discovered through the investigation of the low HDL-C disorder described as Tangier disease and now known to be the result of ABC1 mutations. In order to efflux cholesterol from cells, specific amphipathic helical structures of apoproteins must interact with ABC1. This knowledge has resulted in the production of amphipathic apo A-I mimetic peptides of 18–36 amino acids long that stimulate cholesterol efflux via the ABC1 pathway (196). ABC1 activity can be regulated by several environmental issues including sterols, retinoids, thiazolidinediones, and unsaturated fatty acids (197).
Treatment of Vulnerable Plaques: Current and Future Strategies
Published in Levon Michael Khachigian, High-Risk Atherosclerotic Plaques, 2004
Leonard Kritharides, David Brieger, S. Benedict Freedman, Harry C. Lowe
ABCA1 expression is increased by cholesterol loading and involves oxysteroldependent activation of LXR and RXR transcription factors.178 The clearance of cholesterol once removed from peripheral cells is dependent on transfer reactions in the plasma mediated by lecithin cholesterol acyl transferase (LCAT) and CETP, and then uptake by the liver.179 Several target genes involved in the regulation of cholesterol metabolism are regulated by LXR and RXR and include apoE, ABCA1, LPL, and CETP.178
Gene of the issue: ANO6 and Scott Syndrome
Published in Platelets, 2020
Sarah L. Millington-Burgess, Matthew T. Harper
A missense mutation in the ABCA1 gene was identified in a third Scott patient (VW) (c.6064G>A (ABCA1 R1925Q))[27] which reduced its expression in lymphocytes. This mutation, however, has not been found in any other Scott Syndrome patients and ABCA1 is now known to play a role in cholesterol efflux [28]. ABCA1 mutations cause Tangier disease, patients of which expose normal platelet PS [29,30].
Polydatin inhibits LPS-induced inflammatory response in BV2 microglia by disrupting the formation of lipid rafts
Published in Immunopharmacology and Immunotoxicology, 2021
Shengyu Sun, Yourui Zou, Shaocai Hao, Zhanfeng Niu, Liang Wu
The production of inflammatory mediators were regulated by NF-κB [23]. Meanwhile, NF-κB has been known as a target for the treatment of neurodegenerative diseases [24]. In the present study, our results showed that polydatin significantly attenuated LPS-induced NF-κB activation. As a common target of multiple inflammatory signaling pathways, NF-κB is regulated by a variety of upstream signaling molecules. Activation of PI3K leads to the phosphorylation of phosphatidyl-adenosine, which in turn activates the downstream molecule AKT. Activated AKT activates IκB kinase, which releases NF-κB from the cytoplasm and activates its target gene, and promotes the expression of several inflammatory factors [25]. Phosphorylation of PI3K and AKT were significantly increased after LPS stimulation, and polydatin could inhibit the phosphorylation of PI3K and AKT, suggesting that polydatin can inhibit the activation of NF-κB through the PI3K/Akt signaling pathway. Lipid rafts are plasma membrane microdomains contained with cholesterol and sphingolipids, which play a critical role in signaling pathway. Studies demonstrated that disruption of lipid rafts could block the PI3K/AKT signaling pathway. This study we found polydatin significantly inhibited the formation of lipid rafts by depleting cholesterol. In recent years, a large body of herbal medicines has been reported to have anti-inflammatory effects in BV2 cells [26]. Cudraflavanone B, is isolated from Cudrania tricuspidata, has been reported to inhibit inflammatory response in BV2 cells through suppressing NF-κB signaling pathway [27]. Rhein has been known to inhibit inflammatory mediator production through blocking TLR4 and PI3K/AKT signaling pathways [28]. In this study, our results showed that polydatin could inhibit inflammation in BV2 cells through disrupting lipid rafts formation via attenuating cholesterol level. ABCA1 and ABCG1 are important cholesterol transporters that have the ability to promote cellular phospholipid and cholesterol efflux [29]. In this study, our results showed polydatin dose-dependently increased the expression of ABCA1 and ABCG1. These results suggested polydatin attenuated cholesterol level via up-regulating ABCA1 and ABCG1.
Fe3O4 Nanopowders: Genomic and Apoptotic Evaluations on A549 Lung Adenocarcinoma Cell Line
Published in Nutrition and Cancer, 2020
Ayse Kaplan, Hatice Mehtap Kutlu, Gulsen Akalin Ciftci
The administered cisplatin upregulated 16 genes (BAX, EI24, PEA15, CYFIP2, DKK1, TFPI2, ABCA1, FEZ1, CLDN1, IGFBP7, TP53INP1, FAS, TNFRSF10B, TP53I3, CDKN1A, TNFSF14). Downregulated 9 genes (CCNB1, FGFR3, CDCA5, CCNB2, ASF1B, EIF2C2, FOXC1, ANG, NUCKS1) indicated apoptotic activity. A major role for p53 in the response to chemotherapeutic drugs and regulation of apoptosis has been described. Tumor protein p53 (TP53) is a tumor suppressor gene with a dual role in stress response, regulating a number of genes that coordinately force cells into cell cycle arrest. Cisplatin has induced upregulated of p53 gene in testicular cancer cell lines (30). Cisplatin has induced apoptosis of ovarian cancer A2780s cells by activation of ERK/p53/PUMA signals (31). Accumulating evidence has shown that cisplatin activates the p53-dependent apoptotic pathway, it also induces apoptosis in p53-mutated cancer cells. Bax, has been induced by cisplatin in p53-dependent and -independent manners, respectively in non-small cell lung cancer (32). In our study, Bax and TP53 genes was upregulated by cisplatin but not PUMA gene in A549 cells. This indicate that cisplatin has different effects on different cell lines and has induced different molecular pathways. The IC30 value of Fe3O4 nanopowders upregulated CYFIP1, TFPI2, ABCA1 and CLDN1 genes in A549 cells. The ABCA1 and CLDN1genes were upregulated by IC50 value of cisplatin in A549 cells. In a study, The CYFIP1 gene has been determined as potential tumor suppressor. The downregulated CYFIP1 gene has been observed during the growth of epithelial tumors (33). Therefore, the CYFIP1 gene may be a target gene for cancer treatment. In other study, the TFPI2 gene has been upregulated at CALU-6 and H460 lung cancer cells and It has been thought to be a target of responding to treatment (34). In a study, the TFPI2 gene has been upregulated on kidney cancer cells. In this way, it has been inhibited cell proliferation and has induced apoptosis in kidney cancer cells (35). The upregulated ABCA1 gene has inhibited cell proliferation in LNCaP (human prostate adenocarcinoma) cells (36). The upregulated CLDN1gene has suppressed migration and metastasis in vivo human lung adenocarcinoma cells (37). These findings show that the IC30 value of Fe3O4 nanopowders induced apoptotic pathways by upregulated genes.