Статті в журналах: "Signaling lipid"

1

Wang, Xuemin. "Lipid signaling." Current Opinion in Plant Biology 7, no. 3 (June 2004): 329–36. http://dx.doi.org/10.1016/j.pbi.2004.03.012.

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2

Bickel, Perry E. "Lipid rafts and insulin signaling." American Journal of Physiology-Endocrinology and Metabolism 282, no. 1 (January 1, 2002): E1—E10. http://dx.doi.org/10.1152/ajpendo.2002.282.1.e1.

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Lipid rafts are domains within the plasma membrane that are enriched in cholesterol and lipids with saturated acyl chains. Specific proteins, including many signaling proteins, segregate into lipid rafts, and this process is important for certain signal transduction events in a variety of cell types. Within the past decade, data have emerged from many laboratories that implicate lipid rafts as critical for proper compartmentalization of insulin signaling in adipocytes. A subset of lipid rafts, caveolae, are coated with membrane proteins of the caveolin family. Direct interactions between resident raft proteins (caveolins and flotillin-1) and insulin-signaling molecules may organize these molecules in space and time to ensure faithful transduction of the insulin signal, at least with respect to the glucose-dependent actions of insulin in adipocytes. The in vivo relevance of this model remains to be determined.

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3

Junkins, Sadie, Gabrielle Westenberger, Jacob Sellers, Isabel Martinez, Nabin Ghimire, Cassandra Secunda, Morgan Welch, Urja Patel, Kisuk Min, and Ahmed Lawan. "MKP-2 Deficiency Leads to Lipolytic and Inflammatory Response to Fasting in Mice." Journal of Cellular Signaling 5, no. 1 (2024): 10–23. http://dx.doi.org/10.33696/signaling.5.108.

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The liver plays a crucial role in maintaining homeostasis for lipid and glucose. Hepatic lipid synthesis is regulated by nutritional signals in response to fasting and refeeding. It is known that overnutrition regulates MAPK-dependent pathways that control lipid metabolism in the liver by activating MAPK phosphatase-2 (MKP-2). Uncertainty still exists regarding the regulatory mechanisms and effects of MKP-2 on hepatic response to fasting. We investigated the effect of fasting on the expression of MKP-2 and the impact on hepatic inflammatory response to feeding a high-fat diet (HFD). In this study, we show that fasting stress led to an upregulation of hepatic MKP-2 expression and a corresponding decrease in phosphorylation of p38 MAPK in mouse livers. We discovered that hepatic steatosis brought on by fasting is not effective in MKP-2-deficient livers due in part to a decrease in lipolysis and GLUT2 expression. In response to refeeding a chow or HFD, MKP-2 exhibited differential regulation of hepatic inflammatory cytokines including IL-1β. It has been demonstrated that the mitochondrial carrier uncoupling protein 2 (UCP2) plays a significant role in immune function. We discovered that MKP-2 negatively controls the expression of the UCP2 protein in the liver, modulating the expression of inflammatory cytokines. These results lend credence to the idea that upregulation of MKP-2 is a physiologically relevant response and may help the liver better utilize hepatic lipids while fasting. Collectively, these findings show that MKP-2 modulates lipolysis and hepatic inflammatory response in response to alterations in nutritional status, such as excess nutrients and fasting.

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4

Bazan, Nicolas G. "Synaptic lipid signaling." Journal of Lipid Research 44, no. 12 (September 16, 2003): 2221–33. http://dx.doi.org/10.1194/jlr.r300013-jlr200.

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5

Irvine, R. "Nuclear Lipid Signaling." Science Signaling 2000, no. 48 (September 5, 2000): re1. http://dx.doi.org/10.1126/stke.2000.48.re1.

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6

Irvine, R. F. "Nuclear Lipid Signaling." Science Signaling 2002, no. 150 (September 17, 2002): re13. http://dx.doi.org/10.1126/stke.2002.150.re13.

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7

Höglinger, Doris, André Nadler, Per Haberkant, Joanna Kirkpatrick, Martina Schifferer, Frank Stein, Sebastian Hauke, Forbes D. Porter, and Carsten Schultz. "Trifunctional lipid probes for comprehensive studies of single lipid species in living cells." Proceedings of the National Academy of Sciences 114, no. 7 (February 2, 2017): 1566–71. http://dx.doi.org/10.1073/pnas.1611096114.

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Lipid-mediated signaling events regulate many cellular processes. Investigations of the complex underlying mechanisms are difficult because several different methods need to be used under varying conditions. Here we introduce multifunctional lipid derivatives to study lipid metabolism, lipid−protein interactions, and intracellular lipid localization with a single tool per target lipid. The probes are equipped with two photoreactive groups to allow photoliberation (uncaging) and photo–cross-linking in a sequential manner, as well as a click-handle for subsequent functionalization. We demonstrate the versatility of the design for the signaling lipids sphingosine and diacylglycerol; uncaging of the probe for these two species triggered calcium signaling and intracellular protein translocation events, respectively. We performed proteomic screens to map the lipid-interacting proteome for both lipids. Finally, we visualized a sphingosine transport deficiency in patient-derived Niemann−Pick disease type C fibroblasts by fluorescence as well as correlative light and electron microscopy, pointing toward the diagnostic potential of such tools. We envision that this type of probe will become important for analyzing and ultimately understanding lipid signaling events in a comprehensive manner.

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8

Dowds, C. Marie, Sabin-Christin Kornell, Richard S. Blumberg, and Sebastian Zeissig. "Lipid antigens in immunity." Biological Chemistry 395, no. 1 (January 1, 2014): 61–81. http://dx.doi.org/10.1515/hsz-2013-0220.

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Abstract Lipids are not only a central part of human metabolism but also play diverse and critical roles in the immune system. As such, they can act as ligands of lipid-activated nuclear receptors, control inflammatory signaling through bioactive lipids such as prostaglandins, leukotrienes, lipoxins, resolvins, and protectins, and modulate immunity as intracellular phospholipid- or sphingolipid-derived signaling mediators. In addition, lipids can serve as antigens and regulate immunity through the activation of lipid-reactive T cells, which is the topic of this review. We will provide an overview of the mechanisms of lipid antigen presentation, the biology of lipid-reactive T cells, and their contribution to immunity.

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9

Terao, Ryo, and Hiroki Kaneko. "Lipid Signaling in Ocular Neovascularization." International Journal of Molecular Sciences 21, no. 13 (July 4, 2020): 4758. http://dx.doi.org/10.3390/ijms21134758.

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Vasculogenesis and angiogenesis play a crucial role in embryonic development. Pathological neovascularization in ocular tissues can lead to vision-threatening vascular diseases, including proliferative diabetic retinopathy, retinal vein occlusion, retinopathy of prematurity, choroidal neovascularization, and corneal neovascularization. Neovascularization involves various cellular processes and signaling pathways and is regulated by angiogenic factors such as vascular endothelial growth factor (VEGF) and hypoxia-inducible factor (HIF). Modulating these circuits may represent a promising strategy to treat ocular neovascular diseases. Lipid mediators derived from membrane lipids are abundantly present in most tissues and exert a wide range of biological functions by regulating various signaling pathways. In particular, glycerophospholipids, sphingolipids, and polyunsaturated fatty acids exert potent pro-angiogenic or anti-angiogenic effects, according to the findings of numerous preclinical and clinical studies. In this review, we summarize the current knowledge regarding the regulation of ocular neovascularization by lipid mediators and their metabolites. A better understanding of the effects of lipid signaling in neovascularization may provide novel therapeutic strategies to treat ocular neovascular diseases and other human disorders.

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10

Huwiler, Andrea, and Josef Pfeilschifter. "Hypoxia and lipid signaling." Biological Chemistry 387, no. 10/11 (October 1, 2006): 1321–28. http://dx.doi.org/10.1515/bc.2006.165.

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AbstractSufficient oxygen supply is crucial for the development and physiology of mammalian cells and tissues. When simple diffusion of oxygen becomes inadequate to provide the necessary flow of substrate, evolution has provided cells with tools to detect and respond to hypoxia by upregulating the expression of specific genes, which allows an adaptation to hypoxia-induced stress conditions. The modulation of cell signaling by hypoxia is an emerging area of research that provides insight into the orchestration of cell adaptation to a changing environment. Cell signaling and adaptation processes are often accompanied by rapid and/or chronic remodeling of membrane lipids by activated lipases. This review highlights the bi-directional relation between hypoxia and lipid signaling mechanisms.

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11

Kuźniak, Elżbieta, and Ewa Gajewska. "Lipids and Lipid-Mediated Signaling in Plant–Pathogen Interactions." International Journal of Molecular Sciences 25, no. 13 (July 1, 2024): 7255. http://dx.doi.org/10.3390/ijms25137255.

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Plant lipids are essential cell constituents with many structural, storage, signaling, and defensive functions. During plant–pathogen interactions, lipids play parts in both the preexisting passive defense mechanisms and the pathogen-induced immune responses at the local and systemic levels. They interact with various components of the plant immune network and can modulate plant defense both positively and negatively. Under biotic stress, lipid signaling is mostly associated with oxygenated natural products derived from unsaturated fatty acids, known as oxylipins; among these, jasmonic acid has been of great interest as a specific mediator of plant defense against necrotrophic pathogens. Although numerous studies have documented the contribution of oxylipins and other lipid-derived species in plant immunity, their specific roles in plant–pathogen interactions and their involvement in the signaling network require further elucidation. This review presents the most relevant and recent studies on lipids and lipid-derived signaling molecules involved in plant–pathogen interactions, with the aim of providing a deeper insight into the mechanisms underpinning lipid-mediated regulation of the plant immune system.

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12

Cocco, Lucio, Alberto M. Martelli, Ottavio Barnabei, and Francesco A. Manzoli. "Nuclear inositol lipid signaling." Advances in Enzyme Regulation 41, no. 1 (May 2001): 361–84. http://dx.doi.org/10.1016/s0065-2571(00)00017-0.

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13

Gaur, Pankaj, Maksym Galkin, Sebastian Hauke, Ruslan Redkin, Carolyn Barnes, Volodymyr V. Shvadchak, and Dmytro A. Yushchenko. "Reversible spatial and temporal control of lipid signaling." Chemical Communications 56, no. 73 (2020): 10646–49. http://dx.doi.org/10.1039/d0cc04146g.

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14

Ren, Yuanhao, Wei Wang, Yin Fu, Zhiqiang Liu, Ming Zhao, Likun Xu, Tianyong Zhan, et al. "Comparative Transcriptome Analysis Identifies MAPK Signaling Pathway Associated with Regulating Ovarian Lipid Metabolism during Vitellogenesis in the Mud Crab, Scylla paramamosain." Fishes 8, no. 3 (February 28, 2023): 145. http://dx.doi.org/10.3390/fishes8030145.

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The mud crab, Scylla paramamosain, has abundant nutrients in the ovary, where numerous lipids accumulate during ovarian maturation. However, the mechanism behind the accumulation of lipids in the ovary of mud crab during ovarian maturation is largely unknown. This study conducted a comparative transcriptome analysis of the ovaries of mud crabs at various stages of ovarian maturation. A total of 63.69 Gb of clean data was obtained, with a Q30 of 93.34%, and 81,893 unigenes were identified, including 10,996 differentially expressed genes (DEGs). After KEGG enrichment of these DEGs, MAPK signaling pathway was significantly enriched during vitellogenesis. Moreover, the expression levels of genes involved in carbohydrate, amino acid, and lipid metabolism were found to be higher during vitellogenesis. The two genes (Sp-Eip75B and Sp-Eip78C) that are homologous to the vertebrate gene PPARγ in the PPAR signaling pathway, were identified. Additionally, genes in MAPK signaling pathway might regulate lipid metabolism through PPAR signaling pathway based on Protein-Protein Interaction (PPI) network. These findings suggest that MAPK signaling pathway plays a critical role in lipid metabolism in the ovary during vitellogenesis, which provides new insights into the mechanism of lipid accumulation during ovarian maturation in mud crabs.

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15

Zhang, Cuiping, Ke Wang, Lujie Yang, Ronghua Liu, Yiwei Chu, Xue Qin, Pengyuan Yang, and Hongxiu Yu. "Lipid metabolism in inflammation-related diseases." Analyst 143, no. 19 (2018): 4526–36. http://dx.doi.org/10.1039/c8an01046c.

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Lipidomics is used to describe the complete lipid profile and network of cellular lipid metabolism. Traditionally, lipids are recognized as general membrane construction and energy storage molecules. Now, lipids are regarded as potent signaling molecules that regulate a multitude of cellular responses.

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16

Opazo-Ríos, Lucas, Sebastián Mas, Gema Marín-Royo, Sergio Mezzano, Carmen Gómez-Guerrero, Juan Antonio Moreno, and Jesús Egido. "Lipotoxicity and Diabetic Nephropathy: Novel Mechanistic Insights and Therapeutic Opportunities." International Journal of Molecular Sciences 21, no. 7 (April 10, 2020): 2632. http://dx.doi.org/10.3390/ijms21072632.

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Lipotoxicity is characterized by the ectopic accumulation of lipids in organs different from adipose tissue. Lipotoxicity is mainly associated with dysfunctional signaling and insulin resistance response in non-adipose tissue such as myocardium, pancreas, skeletal muscle, liver, and kidney. Serum lipid abnormalities and renal ectopic lipid accumulation have been associated with the development of kidney diseases, in particular diabetic nephropathy. Chronic hyperinsulinemia, often seen in type 2 diabetes, plays a crucial role in blood and liver lipid metabolism abnormalities, thus resulting in increased non-esterified fatty acids (NEFA). Excessive lipid accumulation alters cellular homeostasis and activates lipogenic and glycogenic cell-signaling pathways. Recent evidences indicate that both quantity and quality of lipids are involved in renal damage associated to lipotoxicity by activating inflammation, oxidative stress, mitochondrial dysfunction, and cell-death. The pathological effects of lipotoxicity have been observed in renal cells, thus promoting podocyte injury, tubular damage, mesangial proliferation, endothelial activation, and formation of macrophage-derived foam cells. Therefore, this review examines the recent preclinical and clinical research about the potentially harmful effects of lipids in the kidney, metabolic markers associated with these mechanisms, major signaling pathways affected, the causes of excessive lipid accumulation, and the types of lipids involved, as well as offers a comprehensive update of therapeutic strategies targeting lipotoxicity.

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17

Srivatsav, Aswin T., Manjari Mishra, and Shobhna Kapoor. "Small-Molecule Modulation of Lipid-Dependent Cellular Processes against Cancer: Fats on the Gunpoint." BioMed Research International 2018 (August 15, 2018): 1–17. http://dx.doi.org/10.1155/2018/6437371.

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Lipid cell membrane composed of various distinct lipids and proteins act as a platform to assemble various signaling complexes regulating innumerous cellular processes which are strongly downregulated or altered in cancer cells emphasizing the still-underestimated critical function of lipid biomolecules in cancer initiation and progression. In this review, we outline the current understanding of how membrane lipids act as signaling hot spots by generating distinct membrane microdomains called rafts to initiate various cellular processes and their modulation in cancer phenotypes. We elucidate tangible drug targets and pathways all amenable to small-molecule perturbation. Ranging from targeting membrane rafts organization/reorganization to rewiring lipid metabolism and lipid sorting in cancer, the work summarized here represents critical intervention points being attempted for lipid-based anticancer therapy and future directions.

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18

Maccarrone, Mauro. "Deciphering Complex Interactions in Bioactive Lipid Signaling." Molecules 28, no. 6 (March 14, 2023): 2622. http://dx.doi.org/10.3390/molecules28062622.

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Lipids are usually viewed as metabolic fuel and structural membrane components. Yet, in recent years, different families of lipids able to act as authentic messengers between cells and/or intracellularly have been discovered. Such lipid signals have been shown to exert their biological activity via specific receptors that, by triggering distinct signal transduction pathways, regulate manifold pathophysiological processes in our body. Here, endogenous bioactive lipids produced from arachidonic acid (AA) and other poly-unsaturated fatty acids will be presented, in order to put into better perspective the relevance of their mutual interactions for health and disease conditions. To this end, metabolism and signal transduction pathways of classical eicosanoids, endocannabinoids and specialized pro-resolving mediators will be described, and the intersections and commonalities of their metabolic enzymes and binding receptors will be discussed. Moreover, the interactions of AA-derived signals with other bioactive lipids such as shingosine-1-phosphate and steroid hormones will be addressed.

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19

Bollag, Wendy B. "Lipid signaling in keratinocytes: Lipin-1 plays a PArt." Journal of Lipid Research 57, no. 4 (February 6, 2016): 523–25. http://dx.doi.org/10.1194/jlr.c067074.

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20

Zhou, Yong, and John F. Hancock. "Lipid Profiles of RAS Nanoclusters Regulate RAS Function." Biomolecules 11, no. 10 (September 30, 2021): 1439. http://dx.doi.org/10.3390/biom11101439.

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The lipid-anchored RAS (Rat sarcoma) small GTPases (guanosine triphosphate hydrolases) are highly prevalent in human cancer. Traditional strategies of targeting the enzymatic activities of RAS have been shown to be difficult. Alternatively, RAS function and pathology are mostly restricted to nanoclusters on the plasma membrane (PM). Lipids are important structural components of these signaling platforms on the PM. However, how RAS nanoclusters selectively enrich distinct lipids in the PM, how different lipids contribute to RAS signaling and oncogenesis and whether the selective lipid sorting of RAS nanoclusters can be targeted have not been well-understood. Latest advances in quantitative super-resolution imaging and molecular dynamic simulations have allowed detailed characterization RAS/lipid interactions. In this review, we discuss the latest findings on the select lipid composition (with headgroup and acyl chain specificities) within RAS nanoclusters, the specific mechanisms for the select lipid sorting of RAS nanoclusters on the PM and how perturbing lipid compositions within RAS nanoclusters impacts RAS function and pathology. We also describe different strategies of manipulating lipid composition within RAS nanoclusters on the PM.

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21

Mesa-Herrera, Taoro-González, Valdés-Baizabal, Diaz, and Marín. "Lipid and Lipid Raft Alteration in Aging and Neurodegenerative Diseases: A Window for the Development of New Biomarkers." International Journal of Molecular Sciences 20, no. 15 (August 4, 2019): 3810. http://dx.doi.org/10.3390/ijms20153810.

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Lipids in the brain are major components playing structural functions as well as physiological roles in nerve cells, such as neural communication, neurogenesis, synaptic transmission, signal transduction, membrane compartmentalization, and regulation of gene expression. Determination of brain lipid composition may provide not only essential information about normal brain functioning, but also about changes with aging and diseases. Indeed, deregulations of specific lipid classes and lipid homeostasis have been demonstrated in neurodegenerative disorders such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). Furthermore, recent studies have shown that membrane microdomains, named lipid rafts, may change their composition in correlation with neuronal impairment. Lipid rafts are key factors for signaling processes for cellular responses. Lipid alteration in these signaling platforms may correlate with abnormal protein distribution and aggregation, toxic cell signaling, and other neuropathological events related with these diseases. This review highlights the manner lipid changes in lipid rafts may participate in the modulation of neuropathological events related to AD and PD. Understanding and characterizing these changes may contribute to the development of novel and specific diagnostic and prognostic biomarkers in routinely clinical practice.

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22

Sibley, D., L. Hazelwood, R. Roof, R. B. Free, Y. Han, and J. Javitch. "Membrane lipid rafts are required for D2 dopamine receptor signaling." European Psychiatry 26, S2 (March 2011): 910. http://dx.doi.org/10.1016/s0924-9338(11)72615-3.

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IntroductionLipid rafts are specialized membrane microdomains enriched in cholesterol and sphingolipids and are important in the organization of receptor-protein complexes and the regulation of signaling.Objective/aimsGiven the emerging significance of lipids with respect to receptor structure and activation, we investigated the role of lipid rafts and membrane cholesterol on D2 dopamine receptor (DAR) signaling. As the D2 DAR is the molecular target for all antipsychotic drugs, more information about its signaling may help refine therapeutics for schizophrenia.MethodsD2 DAR constructs were expressed in HEK293T cells. Sucrose density fractionation resolved lipid rafts from other membrane components. Methyl-β-cyclodextrin (MCD) was used to deplete membrane cholesterol and to disrupt lipid rafts.ResultsDetergent solubilization followed by sucrose gradient centrifugation resolved lipid rafts from heavier membrane fractions. The D2 DAR was equally distributed amongst both the lipid raft and heavier membrane fractions. Pretreatment with MCD, however, eliminated both lipid raft markers and the D2 DAR from lipid raft fractions, although the receptor was still found in heavier membrane fractions. We also found that MCD treatment abolished D2 DAR-mediated inhibition of cAMP accumulation. In contrast D1 DAR-stimulated cAMP accumulation was unaffected by MCD treatment.ConclusionsOur current results show that the D2 DAR is distributed in multiple membrane microdomains, including cholesterol-rich lipid rafts. We found that extraction of cholesterol disrupted lipid rafts and also an eliminated D2 DAR-mediated signaling. Thus, we hypothesize that lipid rafts are critical for D2 DAR signaling to occur.

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23

Béaslas, Olivier, François Torreilles, Pierre Casellas, Dominique Simon, Gérard Fabre, Michel Lacasa, François Delers, Jean Chambaz, Monique Rousset, and Véronique Carrière. "Transcriptome response of enterocytes to dietary lipids: impact on cell architecture, signaling, and metabolism genes." American Journal of Physiology-Gastrointestinal and Liver Physiology 295, no. 5 (November 2008): G942—G952. http://dx.doi.org/10.1152/ajpgi.90237.2008.

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Intestine contributes to lipid homeostasis through the absorption of dietary lipids, which reach the apical pole of enterocytes as micelles. The present study aimed to identify the specific impact of these dietary lipid-containing micelles on gene expression in enterocytes. We analyzed, by microarray, the modulation of gene expression in Caco-2/TC7 cells in response to different lipid supply conditions that reproduced either the permanent presence of albumin-bound lipids at the basal pole of enterocytes or the physiological delivery, at the apical pole, of lipid micelles, which differ in their composition during the interprandial (IPM) or the postprandial (PPM) state. These different conditions led to distinct gene expression profiles. We observed that, contrary to lipids supplied at the basal pole, apical lipid micelles modulated a large number of genes. Moreover, compared with the apical supply of IPM, PPM specifically impacted 46 genes from three major cell function categories: signal transduction, lipid metabolism, and cell adhesion/architecture. Results from this first large-scale analysis underline the importance of the mode and polarity of lipid delivery on enterocyte gene expression. They demonstrate specific and coordinated transcriptional effects of dietary lipid-containing micelles that could impact the structure and polarization of enterocytes and their functions in nutrient transfer.

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24

Brekk, Oeystein Roed, Jonathan R. Honey, Seungil Lee, Penelope J. Hallett, and Ole Isacson. "Cell type-specific lipid storage changes in Parkinson’s disease patient brains are recapitulated by experimental glycolipid disturbance." Proceedings of the National Academy of Sciences 117, no. 44 (October 15, 2020): 27646–54. http://dx.doi.org/10.1073/pnas.2003021117.

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Neurons are dependent on proper trafficking of lipids to neighboring glia for lipid exchange and disposal of potentially lipotoxic metabolites, producing distinct lipid distribution profiles among various cell types of the central nervous system. Little is known of the cellular distribution of neutral lipids in the substantia nigra (SN) of Parkinson’s disease (PD) patients and its relationship to inflammatory signaling. This study aimed to determine human PD SN neutral lipid content and distribution in dopaminergic neurons, astrocytes, and microglia relative to age-matched healthy subject controls. The results show that while total neutral lipid content was unchanged relative to age-matched controls, the levels of whole SN triglycerides were correlated with inflammation-attenuating glycoprotein non-metastatic melanoma protein B (GPNMB) signaling in human PD SN. Histological localization of neutral lipids using a fluorescent probe (BODIPY) revealed that dopaminergic neurons and midbrain microglia significantly accumulated intracellular lipids in PD SN, while adjacent astrocytes had a reduced lipid load overall. This pattern was recapitulated by experimental in vivo inhibition of glucocerebrosidase activity in mice. Agents or therapies that restore lipid homeostasis among neurons, astrocytes, and microglia could potentially correct PD pathogenesis and disease progression.

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25

Torres, Manuel, Sebastià Parets, Javier Fernández-Díaz, Roberto Beteta-Göbel, Raquel Rodríguez-Lorca, Ramón Román, Victoria Lladó, Catalina A. Rosselló, Paula Fernández-García, and Pablo V. Escribá. "Lipids in Pathophysiology and Development of the Membrane Lipid Therapy: New Bioactive Lipids." Membranes 11, no. 12 (November 24, 2021): 919. http://dx.doi.org/10.3390/membranes11120919.

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Membranes are mainly composed of a lipid bilayer and proteins, constituting a checkpoint for the entry and passage of signals and other molecules. Their composition can be modulated by diet, pathophysiological processes, and nutritional/pharmaceutical interventions. In addition to their use as an energy source, lipids have important structural and functional roles, e.g., fatty acyl moieties in phospholipids have distinct impacts on human health depending on their saturation, carbon length, and isometry. These and other membrane lipids have quite specific effects on the lipid bilayer structure, which regulates the interaction with signaling proteins. Alterations to lipids have been associated with important diseases, and, consequently, normalization of these alterations or regulatory interventions that control membrane lipid composition have therapeutic potential. This approach, termed membrane lipid therapy or membrane lipid replacement, has emerged as a novel technology platform for nutraceutical interventions and drug discovery. Several clinical trials and therapeutic products have validated this technology based on the understanding of membrane structure and function. The present review analyzes the molecular basis of this innovative approach, describing how membrane lipid composition and structure affects protein-lipid interactions, cell signaling, disease, and therapy (e.g., fatigue and cardiovascular, neurodegenerative, tumor, infectious diseases).

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26

Cannon, Ashley E., and Kent D. Chapman. "Lipid Signaling through G Proteins." Trends in Plant Science 26, no. 7 (July 2021): 720–28. http://dx.doi.org/10.1016/j.tplants.2020.12.012.

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Rhome, Ryan, and Maurizio Del Poeta. "Lipid Signaling in Pathogenic Fungi." Annual Review of Microbiology 63, no. 1 (October 2009): 119–31. http://dx.doi.org/10.1146/annurev.micro.091208.073431.

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28

Brindley, David N., and Carlos Pilquil. "Lipid phosphate phosphatases and signaling." Journal of Lipid Research 50, Supplement (December 9, 2008): S225—S230. http://dx.doi.org/10.1194/jlr.r800055-jlr200.

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29

Tamiya-Koizumi, K. "Nuclear Lipid Metabolism and Signaling." Journal of Biochemistry 132, no. 1 (July 1, 2002): 13–22. http://dx.doi.org/10.1093/oxfordjournals.jbchem.a003190.

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30

Pozo, Miguel A. Del. "Integrin Signaling and Lipid Rafts." Cell Cycle 3, no. 6 (June 2004): 723–26. http://dx.doi.org/10.4161/cc.3.6.952.

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31

Li, Pin-Lan, and Erich Gulbins. "Lipid Rafts and Redox Signaling." Antioxidants & Redox Signaling 9, no. 9 (September 2007): 1411–16. http://dx.doi.org/10.1089/ars.2007.1736.

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32

Sang, Nan, and Chu Chen. "Lipid Signaling and Synaptic Plasticity." Neuroscientist 12, no. 5 (October 2006): 425–34. http://dx.doi.org/10.1177/1073858406290794.

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33

Shukla, Shivendra D., Grace Y. Sun, W. Gibson Wood, Markku J. Savolainen, Christer Alling, and Jan B. Hoek. "Ethanol and Lipid Metabolic Signaling." Alcoholism: Clinical and Experimental Research 25, s1 (May 2001): 33S—39S. http://dx.doi.org/10.1111/j.1530-0277.2001.tb02370.x.

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Wang, Haibin, and Sudhansu K. Dey. "Lipid signaling in embryo implantation." Prostaglandins & Other Lipid Mediators 77, no. 1-4 (September 2005): 84–102. http://dx.doi.org/10.1016/j.prostaglandins.2004.09.013.

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35

Avraham-Davidi, Inbal, Moshe Grunspan, and Karina Yaniv. "Lipid signaling in the endothelium." Experimental Cell Research 319, no. 9 (May 2013): 1298–305. http://dx.doi.org/10.1016/j.yexcr.2013.01.009.

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36

Shea, John M., and Maurizio Del Poeta. "Lipid signaling in pathogenic fungi." Current Opinion in Microbiology 9, no. 4 (August 2006): 352–58. http://dx.doi.org/10.1016/j.mib.2006.06.003.

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37

Zhang, Yang, Katrin Anne Becker, and Erich Gulbins. "Lipid rafts and redox signaling." Chemistry and Physics of Lipids 160 (August 2009): S2—S3. http://dx.doi.org/10.1016/j.chemphyslip.2009.06.094.

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38

Raben, Daniel M. "Lipid signaling in the nucleus." Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 1761, no. 5-6 (May 2006): 503–4. http://dx.doi.org/10.1016/j.bbalip.2006.05.002.

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39

Raghu, Padinjat, Shweta Yadav, and Naresh Babu Naidu Mallampati. "Lipid signaling in Drosophila photoreceptors." Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 1821, no. 8 (August 2012): 1154–65. http://dx.doi.org/10.1016/j.bbalip.2012.03.008.

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40

Cole-Edwards, Kasie K., and Nicolas G. Bazan. "Lipid Signaling in Experimental Epilepsy." Neurochemical Research 30, no. 6-7 (June 2005): 847–53. http://dx.doi.org/10.1007/s11064-005-6878-4.

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41

Yu, Yi-Hao, and Henry N. Ginsberg. "Adipocyte Signaling and Lipid Homeostasis." Circulation Research 96, no. 10 (May 27, 2005): 1042–52. http://dx.doi.org/10.1161/01.res.0000165803.47776.38.

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42

Rao, Rakesh, Barbara Logan, Kathy Forrest, Thomas L. Roszman, and Jens Goebel. "Lipid rafts in cytokine signaling." Cytokine & Growth Factor Reviews 15, no. 2-3 (April 2004): 103–10. http://dx.doi.org/10.1016/j.cytogfr.2004.01.003.

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43

Allegra, Alessandro, Giuseppe Murdaca, Giuseppe Mirabile, and Sebastiano Gangemi. "Protective Effects of High-Density Lipoprotein on Cancer Risk: Focus on Multiple Myeloma." Biomedicines 12, no. 3 (February 24, 2024): 514. http://dx.doi.org/10.3390/biomedicines12030514.

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Lipid metabolism is intrinsically linked to tumorigenesis. And one of the most important characteristics of cancer is the modification of lipid metabolism and its correlation with oncogenic signaling pathways within the tumors. Because lipids function as signaling molecules, membrane structures, and energy sources, lipids are essential to the development of cancer. Above all, the proper immune response of tumor cells depends on the control of lipid metabolism. Changes in metabolism can modify systems that regulate carcinogenesis, such as inflammation, oxidative stress, and angiogenesis. The dependence of various malignancies on lipid metabolism varies. This review delves into the modifications to lipid metabolism that take place in cancer, specifically focusing on multiple myeloma. The review illustrates how changes in different lipid pathways impact the growth, survival, and drug-responsiveness of multiple myeloma cells, in addition to their interactions with other cells within the tumor microenvironment. The phenotype of malignant plasma cells can be affected by lipid vulnerabilities, and these findings offer a new avenue for understanding this process. Additionally, they identify novel druggable pathways that have a major bearing on multiple myeloma care.

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44

Ediriweera, Meran Keshawa, Jeong Yong Moon, Yen Thi-Kim Nguyen, and Somi Kim Cho. "10-Gingerol Targets Lipid Rafts Associated PI3K/Akt Signaling in Radio-Resistant Triple Negative Breast Cancer Cells." Molecules 25, no. 14 (July 10, 2020): 3164. http://dx.doi.org/10.3390/molecules25143164.

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10-Gingerol is a major phenolic lipid found in the rhizomes of ginger (Zingiber officinale). Being amphiphilic in nature, phenolic lipids have the ability to incorporate into cell membranes and modulate membrane properties. The purpose of the present study was to evaluate the effects of 10-gingerol on lipid raft/membrane raft modulation in radio-resistant triple negative breast cancer (MDA-MB-231/IR) cells. The effects of 10-gingerol on MDA-MB-231/IR cells’ proliferation, clonogenic growth, migration, and invasion were assayed using MTT, colony formation, cell migration, and invasion assays, respectively. Sucrose density gradient centrifugation was used to extract lipid rafts. Western blotting and immunofluorescence were employed to assess the effects of 10-gingerol on lipid raft/membrane raft modulation and lipid rafts-associated PI3K/Akt signaling. Cholesterol measurements were carried out using a commercially available kit. 10-gingerol suppressed the proliferation, migration, invasion, and induced apoptosis through targeting the PI3K/Akt signaling pathway in MDA-MB-231/IR cells. Moreover, 10-gingerol was found to modulate the lipid rafts of MDA-MB-231/IR cells and attenuate the key PI3K/Akt signaling components in lipid rafts. The cholesterol content of the lipid rafts and rafts-resident Akt signaling were also affected by exposure to 10-gingerol. The results of the present study highlight rafts-associated PI3K/Akt signaling as a new target of 10-gingerol in MDA-MB-231/IR cells, thus rationalizing a new rafts-mediated treatment approach for radio-resistant triple negative breast cancer cells.

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45

Torres, Manuel, Catalina Ana Rosselló, Paula Fernández-García, Victoria Lladó, Or Kakhlon, and Pablo Vicente Escribá. "The Implications for Cells of the Lipid Switches Driven by Protein–Membrane Interactions and the Development of Membrane Lipid Therapy." International Journal of Molecular Sciences 21, no. 7 (March 27, 2020): 2322. http://dx.doi.org/10.3390/ijms21072322.

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The cell membrane contains a variety of receptors that interact with signaling molecules. However, agonist–receptor interactions not always activate a signaling cascade. Amphitropic membrane proteins are required for signal propagation upon ligand-induced receptor activation. These proteins localize to the plasma membrane or internal compartments; however, they are only activated by ligand-receptor complexes when both come into physical contact in membranes. These interactions enable signal propagation. Thus, signals may not propagate into the cell if peripheral proteins do not co-localize with receptors even in the presence of messengers. As the translocation of an amphitropic protein greatly depends on the membrane’s lipid composition, regulation of the lipid bilayer emerges as a novel therapeutic strategy. Some of the signals controlled by proteins non-permanently bound to membranes produce dramatic changes in the cell’s physiology. Indeed, changes in membrane lipids induce translocation of dozens of peripheral signaling proteins from or to the plasma membrane, which controls how cells behave. We called these changes “lipid switches”, as they alter the cell’s status (e.g., proliferation, differentiation, death, etc.) in response to the modulation of membrane lipids. Indeed, this discovery enables therapeutic interventions that modify the bilayer’s lipids, an approach known as membrane-lipid therapy (MLT) or melitherapy.

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46

Michalik, Liliane, and Walter Wahli. "PPARs Mediate Lipid Signaling in Inflammation and Cancer." PPAR Research 2008 (2008): 1–15. http://dx.doi.org/10.1155/2008/134059.

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Lipid mediators can trigger physiological responses by activating nuclear hormone receptors, such as the peroxisome proliferator-activated receptors (PPARs). PPARs, in turn, control the expression of networks of genes encoding proteins involved in all aspects of lipid metabolism. In addition, PPARs are tumor growth modifiers, via the regulation of cancer cell apoptosis, proliferation, and differentiation, and through their action on the tumor cell environment, namely, angiogenesis, inflammation, and immune cell functions. Epidemiological studies have established that tumor progression may be exacerbated by chronic inflammation. Here, we describe the production of the lipids that act as activators of PPARs, and we review the roles of these receptors in inflammation and cancer. Finally, we consider emerging strategies for therapeutic intervention.

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47

Cerasuolo, Michele, Irene Di Meo, Maria Chiara Auriemma, Giuseppe Paolisso, Michele Papa, and Maria Rosaria Rizzo. "Exploring the Dynamic Changes of Brain Lipids, Lipid Rafts, and Lipid Droplets in Aging and Alzheimer’s Disease." Biomolecules 14, no. 11 (October 26, 2024): 1362. http://dx.doi.org/10.3390/biom14111362.

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Aging induces complex changes in the lipid profiles across different areas of the brain. These changes can affect the function of brain cells and may contribute to neurodegenerative diseases such as Alzheimer’s disease. Research shows that while the overall lipid profile in the human brain remains quite steady throughout adulthood, specific changes occur with age, especially after the age of 50. These changes include a slow decline in total lipid content and shifts in the composition of fatty acids, particularly in glycerophospholipids and cholesterol levels, which can vary depending on the brain region. Lipid rafts play a crucial role in maintaining membrane integrity and facilitating cellular signaling. In the context of Alzheimer’s disease, changes in the composition of lipid rafts have been associated with the development of the disease. For example, alterations in lipid raft composition can lead to increased accumulation of amyloid β (Aβ) peptides, contributing to neurotoxic effects. Lipid droplets store neutral lipids and are key for cellular energy metabolism. As organisms age, the dynamics of lipid droplets in the brain change, with evidence suggesting a decline in metabolic activity over time. This reduced activity may lead to an imbalance in lipid synthesis and mobilization, contributing to neurodegenerative processes. In model organisms like Drosophila, studies have shown that lipid metabolism in the brain can be influenced by diet and insulin signaling pathways, crucial for maintaining metabolic balance. The interplay between lipid metabolism, oxidative stress, and inflammation is critical in the context of aging and Alzheimer’s disease. Lipid peroxidation, a consequence of oxidative stress, can lead to the formation of reactive aldehydes that further damage neurons. Inflammatory processes can also disrupt lipid metabolism, contributing to the pathology of AD. Consequently, the accumulation of oxidized lipids can affect lipid raft integrity, influencing signaling pathways involved in neuronal survival and function.

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48

Havranek, Katherine E., Judith Mary Reyes Ballista, Kelly Marie Hines, and Melinda Ann Brindley. "Untargeted Lipidomics of Vesicular Stomatitis Virus-Infected Cells and Viral Particles." Viruses 14, no. 1 (December 21, 2021): 3. http://dx.doi.org/10.3390/v14010003.

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The viral lifecycle is critically dependent upon host lipids. Enveloped viral entry requires fusion between viral and cellular membranes. Once an infection has occurred, viruses may rely on host lipids for replication and egress. Upon exit, enveloped viruses derive their lipid bilayer from host membranes during the budding process. Furthermore, host lipid metabolism and signaling are often hijacked to facilitate viral replication. We employed an untargeted HILIC-IM-MS lipidomics approach and identified host lipid species that were significantly altered during vesicular stomatitis virus (VSV) infection. Many glycerophospholipid and sphingolipid species were modified, and ontological enrichment analysis suggested that the alterations to the lipid profile change host membrane properties. Lysophosphatidylcholine (LPC), which can contribute to membrane curvature and serve as a signaling molecule, was depleted during infection, while several ceramide sphingolipids were augmented during infection. Ceramide and sphingomyelin lipids were also enriched in viral particles, indicating that sphingolipid metabolism is important during VSV infection.

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49

Yang, Wenlin, Nikee Awasthee, Qi Chen, Seth Hale, and Daiqing Liao. "Abstract 4451: Regulation of lipid metabolism and ferroptosis by DAXX." Cancer Research 84, no. 6_Supplement (March 22, 2024): 4451. http://dx.doi.org/10.1158/1538-7445.am2024-4451.

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Abstract Intracellular lipid production in cancer cells supplies lipids to synthesize cell membranes and signaling molecules during rapid cell proliferation and tumor growth. Cancer cells also utilize fatty acid oxidation (FAO) to generate ATP to meet their energy demand. Notably, lipid metabolites can inhibit and trigger ferroptosis due to iron-dependent oxidation of polyunsaturated fatty acids (PUFAs). Therefore, identifying regulators that maintain the intricate balance of lipid biosynthesis required for cell proliferation and survival is critical in cancer biology and therapy. Lipid metabolism is regulated by two oncogenic signaling pathways: the RAS-RAF-MEK-MAPK and the mammalian target of rapamycin (mTOR) pathways. About 30% of all cancers harbor constitutively active mutations in KRAS, HRAS, or NRAS, resulting in hyperactive RAS-RAF-MEK-MAPK signaling to drive tumorigenesis, metastatic progression, immune evasion, and resistance to therapy. KRAS regulates lipid uptake, lipid synthesis, and FAO. mTOR is a serine/threonine kinase acting as a key intracellular signaling hub to regulate nutrient homeostasis, metabolism, protein synthesis, and autophagy. The mTORC1 complex promotes lipogenesis. The RAS and mTOR signaling pathways exhibit both positive and negative cross-regulation. The coordinated activity of both pathways is critical to sustained tumor growth. Notably, mTORC1 signaling inhibition enhances RAS-RAF-MEK-MAPK signaling to promote cancer cell survival and proliferation. Furthermore, constitutive mTORC1 signaling induces cell death when the supply of unsaturated FAs is limited. However, the molecular link for coordinating the activity of the RAS and mTOR signaling pathways remains poorly defined. Death domain-associated protein (DAXX) is essential for mouse embryonic development and has ill-defined pro-cell survival functions. Our lab has a long-standing interest in deciphering DAXX’s complex biological functions. Our recent study shows that DAXX drives tumorigenesis by promoting lipogenic gene expression and lipid synthesis through interacting with sterol regulatory element-binding proteins SREBP1 and SREBP2 (SREBP1/2) (Mahmud et al., 2023, PMID 37045819). Unexpectedly, our new data reveal that DAXX inhibits ferroptosis. Significantly, phosphorylation via RAS signaling appears to regulate DAXX’s activity in lipid synthesis and resistance to ferroptosis. Remarkably, disruption of DAXX-mediated lipid synthesis potentiates ferroptosis due to mTORC1 activity. Based on these observations, we propose that stimulated by the RAS-RAF-MEK-MAPK oncogenic signaling, DAXX promotes tumorigenesis through upregulating genes for lipid synthesis and resistance to ferroptosis, and that the lack of DAXX-mediated lipid synthesis leads to sensitization of cells to ferroptosis due to mTORC1’s proliferative effects. (Supported by FDOH grant 23K03). Citation Format: Wenlin Yang, Nikee Awasthee, Qi Chen, Seth Hale, Daiqing Liao. Regulation of lipid metabolism and ferroptosis by DAXX [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 4451.

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Liu, Zhenjiang, Lu Gan, Xiaobo Yang, Zhenzhen Zhang, and Chao Sun. "Hydrodynamic tail vein injection of SOCS3 eukaryotic expression vector in vivo promoted liver lipid metabolism and hepatocyte apoptosis in mouse." Biochemistry and Cell Biology 92, no. 2 (April 2014): 119–25. http://dx.doi.org/10.1139/bcb-2013-0117.

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Suppressor of cytokine signaling 3 (SOCS3), a signal transduction cytokine, is involved in lipid metabolism as well as in cell proliferation, differentiation, apoptosis, and so on. To explore the effects of SOCS3 on apoptosis and lipid metabolism in liver, we used a simple effective method named hydrodynamic tail vein injection to overexpress SOCS3. Then orbital blood was obtained for the assessment of blood lipid after injection. Lipid metabolism related genes were detected by Western blot after the determination of serum lipids. Meanwhile, liver cell apoptosis was observed by Hoechst and TUNEL staining and the expression of apoptosis related proteins Bax, Bcl-2, and Caspase3 were detected as well as the JAK2/STAT3 signaling pathway. In addition, we also demonstrated the effect of SOCS3 in prime hepatocyte by overexpression or interference of SOCS3 along with SD1008, which is a specific inhibitor of the JAK2/STAT3 signaling pathway. Taken together, all the results indicated that SOCS3 promoted lipid synthesis in mice liver and promoted hepatocyte apoptosis by inhibiting the activation of the JAK2/STAT3 signaling pathway, however the detailed regulation mechanism had not yet been fully understood and needs further study.

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