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Host Defense and Parasite Evasion
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2023
Eric S. Loker, Bruce V. Hofkin
These examples feature parasites that normally infect APCs. P. falciparum, of course, first targets hepatocytes and then erythrocytes for intracellular replication. Yet since the late 1990s, it has been known that infected erythrocytes can somehow reduce MHC II expression on dendritic cells. Such dendritic cells also secrete an altered cytokine profile, which, as we will see shortly, results in a less protective adaptive immune response. As discussed in Chapter 3 (see p. 119), infected erythrocytes express erythrocyte membrane protein 1 (PfEMPl), on their surfaces. This protein serves as a ligand for CD36, found on the surface of dendritic cells. Such binding initiates an intracellular signal that inhibits MHC II expression. The clinical significance of this is suggested by the observation that patients with either severe or mild malaria have reduced MHC II expression on dendritic cells as compared to healthy controls.
Molecular sport nutrition
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Mark Hearris, Nathan Hodson, Javier Gonzalez, James P. Morton
For circulatory fatty acids, derived from either the ingestion of a high-fat meal or adipose tissue lipolysis, to enter the muscle cell they are transported across the cell membrane by various fatty acid transporters. These include fatty acid translocase (also known as CD36) and fatty acid binding protein (FABP), whereby a greater presence of fatty acid transporters on the muscle membrane results in a greater uptake of fatty acids into the muscle. In this regard, the adoption of a high-fat diet can increase the content of these transporters and allow for a greater delivery of fatty acids into the muscle. Indeed, as little as five days of fat adaptation is sufficient to increase resting gene expression and total protein content of the fatty acid transporter CD36 (25). These responses do, however, occur in the absence of changes in FABPpm, suggesting that an increase in CD36 is the primary mechanism by which fat adaptation occurs (25). Furthermore, the increase in CD36 content that is achieved with fat adaptation is rapidly reversed within just one day of consuming a high CHO diet (26), demonstrating how sensitive this transport protein is to changes in dietary fat intake.
Carnitine palmitoyl transferase I deficiency
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop
The fatty acid transport protein FAT/CD36 found in the plasma membrane may also contribute to the regulation of fatty acid oxidation. FAT/CD36 KO mice are unaffected by sulfo-N-succinimidyloleate which inhibits palmitate transport across the plasma membrane [36]. Regulation of mitochondrial fatty acid oxidation is particularly relevant during the metabolic demands of muscle contraction. The CPT IA gene on chromosome 11q13.1-13.5 [37] is expressed in liver, kidney, pancreas, ovary, leukocytes, and fibroblasts [16]. The gene spans 60 kb and contains 20 exons. The first mutation described [15] was a missense (D454G) change, which when expressed, had 2 percent of wild-type activity. Other mutations identified [16] include Q100X, which would predict an early truncation of the protein, H414V, and Y498C, which affect highly conserved sequences in the catalytic core of the enzyme. An 8-kb deletion encompassing intron 14 to exon 17 led to loss of the mRNA [16]. The rarity of the disease and the general severity of phenotype have made genotype–phenotype correlations difficult, but the mutation leading to P479L resulted in a late onset disease in which there was proximal myopathy. Homozygosity for the 1436 (C > T) mutation was identified [38] in patients with deficient CPT 1A enzyme. In a Japanese newborn, two novel mutations, p.R446X and p.G719D were found [39]. Four novel mutations were found [40] in patients with severe disease: G405W, R316R, and F343V.
A review of protein-protein interaction and signaling pathway of Vimentin in cell regulation, morphology and cell differentiation in normal cells
Published in Journal of Receptors and Signal Transduction, 2022
Danial Hashemi Karoii, Hossein Azizi
Furthermore, they show the significance of Vimentin in regulating Notch signaling in angiogenesis development and that Vimentin plays a variety of essential functions in the stimulation of various angiogenic processes. They provide insight into the role of Vimentin in atherogenesis. The impairment of increased oxidative stress indicators [13], extracellular lipoprotein absorption [50], increased GLUT1-mediated glucose uptake [13], increased proinflammatory cytokine production, increased CD36 expression [51], and NFB activation is explained by the study of bone marrow-derived macrophages from Vim/mice [23,52]. This discovered increased CD36 expression on macrophages in atherosclerotic lesions in vivo, which we linked to the inflammatory response. Atherogenesis is initiated by the accumulation of atherogenic lipoproteins in the subendothelial space [7,52]. The lipoproteins (retained) are altered, resulting in an inflammatory reaction. Surprisingly, the authors show that, despite higher vascular inflammation, Vim/mice had much less atherosclerosis [13,53].
A complete proteomic profile of human and bovine milk exosomes by liquid chromatography mass spectrometry
Published in Expert Review of Proteomics, 2021
Kanchan Manohar Vaswani, Hassendrini Peiris, Yong Qin Koh, Rebecca J. Hill, Tracy Harb, Buddhika J. Arachchige, Jayden Logan, Sarah Reed, Peter S. W. Davies, Murray D. Mitchell
Both the human and bovine milk exosomes contained Platelet glycoprotein four in the top 20 abundant list. This protein, also called CD36, is involved in pathogen recognition, phagocytosis, and pathogen-induced signaling [32] and is a receptor for a range of ligands (such as TLR4 and hence LPS recognition). The formation of CD36 ligand-binding complexes promotes signal transduction and internalization into cells. Since exosomes have been identified as novel signal transducers, this can be explored further since within cells CD36 responses have been shown to play roles in angiogenesis, inflammatory responses, fatty acid metabolism, taste, and dietary fat processing in the intestine, participating in muscle lipid utilization, adipose energy storage, and gut fat absorption and may also serve as a therapeutic target for reducing the postprandial hypertriglyceridemia linked to cardiovascular issues [33–35]. Wilcox C.P. et al. report that there is a form of CD36 that is distinct from the type found in MFGM [36]. Since CD36 is found within the MFGM as well as in the exosomes of both human and bovine milk, it will be important to study further how similar or different its function is compared to its function in cells. Garcia et al. 2019 identified that the CD36 in circulating exosomes increased postprandially [37] which is interesting as studies need to confirm if this is the case after infants ingest different types of milk.
CD36 as a target for metabolic modulation therapy in cardiac disease
Published in Expert Opinion on Therapeutic Targets, 2021
Jan F.C. Glatz, Fang Wang, Miranda Nabben, Joost J.F.P. Luiken
Of major importance is the specificity of the approach to alter CD36 functioning. First, CD36 is a scavenger receptor with a broad cell-type expression, being found not only in cardiac and skeletal myocytes, but also in adipocytes, intestinal enterocytes, macrophages, and monocytes, while its expression in the liver is induced upon high fat consumption [50]. Second, CD36 not only binds long-chain fatty acids, but also is a receptor for oxidized low-density lipoproteins, thrombospondin, and collagen, apoptotic cells, and erythrocytes infected with Plasmodium falciparum [reviewed in 50]. As a result, CD36 is a multifunctional protein involved in a variety of (mostly lipid-related) pathways. Therefore, when altering CD36 presence or functioning by direct inhibition of the protein, the possibility of introducing unwanted side effects should always be considered and evaluated. For instance, it has been found that blocking CD36 inhibits macrophage phagocytosis of dead myocytes and neutrophils resulting in impaired removal of debris and adverse left ventricular remodeling post-myocardial infarction [51]. However, this limitation may be overcome by indirect approaches to alter CD36 presence in the plasma membrane, i.e. by targeting the subcellular recycling of CD36 between endosomes and the plasma membrane, and do so in a tissue-specific manner [52] as explained below.