Chylomicron assembly and catabolism: role of apolipoproteins and receptors

Hussain, M. Mahmood; Kancha, Ravi K.; Zhou, Zhangyin; Luchoomun, Jayraz; Zu, Hongya; Bakillah, Ahmed

doi:10.1016/0005-2760(96)00041-0

Cited by 164 publications

(14 citation statements)

References 268 publications

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“…ROL can be directly absorbed by the mucosal cell of the small intestine [40], while REs are further hydrolyzed for intestinal absorption by enzymes such as pancreatic triglyceride lipase and pancreatic lipase-related protein 2 [32,41]. The absorbed ROL is re-esterified by transmembrane lecithin retinol acyltransferase (LRAT) [42,43] and incorporated into chylomicrons that are transferred to hepatic stellate cells [44,45] for storage or taken up by other organs/tissues [33,46,47].…”

Section: Generation Of Ramentioning

confidence: 99%

All-trans Retinoic Acid as a Versatile Cytosolic Signal Modulator Mediated by CRABP1

Nagpal

2019

IJMS

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All-trans retinoic acid (AtRA), an active metabolite of vitamin A, is recognized for its classical action as an endocrine hormone that triggers genomic effects mediated through nuclear receptors RA receptors (RARs). New evidence shows that atRA-mediated cellular responses are biphasic with rapid and delayed responses. Most of these rapid atRA responses are the outcome of its binding to cellular retinoic acid binding protein 1 (CRABP1) that is predominantly localized in cytoplasm and binds to atRA with a high affinity. This review summarizes the most recent studies of such non-genomic outcomes of atRA and the role of CRABP1 in mediating such rapid effects in different cell types. In embryonic stem cells (ESCs), atRA-CRABP1 dampens growth factor sensitivity and stemness. In a hippocampal neural stem cell (NSC) population, atRA-CRABP1 negatively modulates NSC proliferation and affects learning and memory. In cardiomyocytes, atRA-CRABP1 prevents over-activation of calcium-calmodulin-dependent protein kinase II (CaMKII), protecting heart function. These are supported by the fact that CRABP1 gene knockout (KO) mice exhibit multiple phenotypes including hippocampal NSC expansion and spontaneous cardiac hypertrophy. This indicates that more potential processes/signaling pathways involving atRA-CRABP1 may exist, which remain to be identified.

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Section: Generation Of Ramentioning

confidence: 99%

All-trans Retinoic Acid as a Versatile Cytosolic Signal Modulator Mediated by CRABP1

Nagpal

2019

IJMS

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“…Due to their structural similarities and localization on the surface of lipoproteins, sphingolipid catabolism is expected to be very similar to phospholipids and free cholesterol. Nascent plasma lipoproteins are hydrolyzed at endothelial cell surfaces by the action of lipoprotein lipases resulting in the hydrolysis of triglycerides and phospholipids and shedding of some of the surface components [31,32]. It is unknown whether sphingolipids remain associated with lipoproteins during and after lipase action.…”

Section: Synthesis and Conversion Of Ceramides Into Different Sphingomentioning

confidence: 99%

Mechanisms involved in cellular ceramide homeostasis

Hussain

Jin

2012

Nutr Metab (Lond)

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Sphingolipids are ubiquitous and critical components of biological membranes. Their biosynthesis starts with soluble precursors in the endoplasmic reticulum and culminates in the Golgi complex and plasma membrane. Ceramides are important intermediates in the biosynthesis of sphingolipids, such as sphingomyelin, and their overload in the membranes is injurious to cells. The major product of ceramide metabolism is sphingomyelin. We observed that sphingomyelin synthase (SMS) 1 or SMS2 deficiencies significantly decreased plasma and liver sphingomyelin levels. However, SMS2 but not SMS1 deficiency increased plasma ceramides. Surprisingly, SMS1 deficiency significantly increased glucosylceramide and ganglioside GM3, but SMS2 deficiency did not. To explain these unexpected findings about modest to no significant changes in ceramides and increases in other sphingolipids after the ablation of SMS1, we hypothesize that cells have evolved several organelle specific mechanisms to maintain ceramide homeostasis. First, ceramides in the endoplasmic reticulum membranes are controlled by its export to Golgi by protein mediated transfer. Second, in the Golgi, ceramide levels are modulated by their enzymatic conversion to different sphingolipids such as sphingomyelin, and glucosylceramides. Additionally, these sphingolipids can become part of triglyceride-rich apolipoprotein B-containing lipoproteins and be secreted. Third, in the plasma membrane ceramide levels are maintained by ceramide/sphingomyelin cycle, delivery to lysosomes, and efflux to extracellular plasma acceptors. All these pathways might have evolved to ensure steady cellular ceramide levels.

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“…For exploration in mice, we chose the homozygous apolipoprotein E-deficient mouse strain (ApoE −/− ), which has long been used as a model for atherogenesis. ApoE plays a central role in lipoprotein metabolism and is required for the clearance of diet-derived chylomicrons and liver-derived vLDL by the liver [32]. Consequently, mice lacking ApoE can be used as an animal model of hyperlipidemia (especially hypercholesterolemia) and resulting atherosclerosis, which can be accelerated by feeding a high-fat (western-type) diet [33].…”

Section: Discussionmentioning

confidence: 99%

Monitoring Endothelin-A Receptor Expression during the Progression of Atherosclerosis

et al. 2020

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Cardiovascular disease remains the most frequent cause of death worldwide. Atherosclerosis, an underlying cause of cardiovascular disease, is an inflammatory disorder associated with endothelial dysfunction. The endothelin system plays a crucial role in the pathogenesis of endothelial dysfunction and is involved in the development of atherosclerosis. We aimed to reveal the expression levels of the endothelin-A receptor (ETAR) in the course of atherogenesis to reveal possible time frames for targeted imaging and interventions. We used the ApoE−/− mice model and human specimens and evaluated ETAR expression by quantitative rtPCR (qPCR), histology and fluorescence molecular imaging. We found a significant upregulation of ETAR after 22 weeks of high-fat diet in the aortae of ApoE−/− mice. With regard to translation to human disease, we applied the fluorescent probe to fresh explants of human carotid and femoral artery specimens. The findings were correlated with qPCR and histology. While ETAR is upregulated during the progression of early atherosclerosis in the ApoE−/− mouse model, we found that ETAR expression is substantially reduced in advanced human atherosclerotic plaques. Moreover, those expression changes were clearly depicted by fluorescence imaging using our in-house designed ETAR-Cy 5.5 probe confirming its specificity and potential use in future studies.

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Chylomicron assembly and catabolism: role of apolipoproteins and receptors

Cited by 164 publications

References 268 publications

All-trans Retinoic Acid as a Versatile Cytosolic Signal Modulator Mediated by CRABP1

All-trans Retinoic Acid as a Versatile Cytosolic Signal Modulator Mediated by CRABP1

Mechanisms involved in cellular ceramide homeostasis

Monitoring Endothelin-A Receptor Expression during the Progression of Atherosclerosis

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