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PubMed2002

Effect of bowel resection and high-fat diet on heart CD36/fatty-acid translocase expression in a rat model of short-bowel syndrome.

Long-chain fatty acids (LCFA) are the major energy substrates for the heart. In short-bowel syndrome (SBS), LCFA delivery to the myocardium decreases due to fat malabsorption. Fatty-acid translocase (FAT)/CD36 has recently been identified as a LCFA-binding protein in heart tissue. To determine the effects of bowel resection and a high-fat diet (HFD) on myocardial CD36 expression, male Sprague-Dawley rats were randomly assigned to one of three groups: sham rats fed normal chow (Sham-NC); SBS rats fed NC (SBS-NC), and SBS rats fed a HFD (SBS-HFD). Control rats underwent transection and anastomosis; SBS animals underwent 75% small-bowel resection. Rats were killed at 3 or 14 days. Total body weight, heart weight, heart-tissue total lipid, serum cholesterol, and triglycerides were determined at death. Total RNA from the myocardium was extracted using TRIZOL reagent. Northern-blot analysis was used to determine FAT/CD36 mRNA. Statistical significance was determined by Student's t-test with P values below 0.05 considered significant. SBS-NC and SBS-HFD rats had significantly lower body weights compared with Sham-NC animals. The heart weights and myocardial total lipid did not vary among experimental groups. Decreases in plasma triglycerides (38.2 +/- 3.8 vs 58.8 +/- 5.5 mg/dl, P < 0.05) and cholesterol (38.2 +/- 6.9 vs 55.3 +/- 8.2 mg/dl, P < 0.05) in SBS-NC compared to Sham-NC rats on day 3 was accompanied by a twofold increase ( P < 0.05) in myocardial CD36/FAT mRNA levels. Early exposure to HFD led to increased (vs SBS-NC) plasma cholesterol (82.9 +/- 5.7 vs 38.2 +/- 6.9 mg/dl, P < 0.05) and triglycerides (62.5 +/- 15.6 vs 38.2 +/- 3.8 mg/dl, P < 0.05), and a concomitant decrease in CD36/FAT mRNA levels (45.1 +/- 17.8 vs 86.6 +/- 15%, respectively, P < 0.05). Plasma lipid concentration and myocardial CD36/FAT mRNA levels on day 14 were not significantly different among the experimental groups. In this rat model of SBS, the heart thus reacts to decreased LCFA delivery by increased tissue CD36/FAT mRNA levels and, consequently, active LCFA uptake. A HFD increased plasma lipid concentrations and decreased CD36/FAT levels.

Animals↗
PubMed2001

Effect of low fat diet on lipid absorption and fatty-acid transport following bowel resection.

Low-fat diets (LFD) are used extensively in many different clinical conditions. However, the effect of this diet on lipid absorption and cellular long-chain fatty-acid (LCFA) transport is unknown. Fatty-acid translocase (FAT), the rat homologue of human CD36, is one of several LCFA plasma-membrane transport proteins that may play an important role in intestinal lipid uptake. The purpose of this study was to investigate the effects of a LFD on intestinal expression of FAT/CD36, enterocyte fatty-acid transport, and in-vivo lipid absorption in rats following bowel resection. Adult male Sprague-Dawley rats were divided into five experimental groups: normal rats fed normal chow(NR-NC) (10 kcal% fat), normal rats fed a LFD (NR-LFD) (3 kcal% fat), sham rats fed normal chow (Sham-NC), short-bowel syndrome rats fed normal chow (SBS-NC), and SBS rats fed a LFD (SBS-LFD). SBS rats underwent 75% small-bowel resection, while sham animals underwent bowel transection and reanastomosis. Food intake, fecal mass, and fecal fat were measured over the last 3 days before death on day 14. Final body weight, plasma lipids and protein, and tissue total lipids in liver, adipose tissue, and intestine were determined at death. Total RNA from the mucosa of the duodenum, jejunum, and ileum was extracted for Northern blot analysis to determine fatty-acid translocase (FAT)/CD36 mRNA levels. An established cellular LCFA transport assay was used to determine isolated enterocyte [3H]-oleate uptake. Students t-test was used to determine statistical significance (P < 0.05). NR-LFD rats demonstrated a small increase in overall food absorption and no change in fat absorption compared to NR-NC animals. A significant decrease in FAT/CD36 mRNA levels was seen in the duodenum and jejunum in NF-LFD rats (vs NR-NC) and was accompanied by reduced LCFA transport by isolated enterocytes from the jejunum and ileum. SBS-LFD rats demonstrated decreased FAT/CD36 mRNA levels in all three segments and a concomitant decrease in LCFA uptake enterocytes compared to the SBS-NC group. In addition, SBS-LFD rats showed significantly lower final body weight and plasma lipids compared to SBS-NC animals.

Animals↗
PubMed2006

Intra- and interindividual variation in gene expression in human adipose tissue.

Adipose tissue is a highly plastic tissue with an important endocrine and metabolic function. To understand its role in human health and disease, it is necessary to understand the extent of variation and the specific differences within and between different depots and subjects. We employed cDNA microarray analysis to investigate this in human subjects ranging from lean to mildly obese. We observe (1) high similarity between different samples of one adipose depot, (2) only small differences between the subcutaneous and visceral adipose tissue depot and (3) larger differences in gene expression between different individuals (per depot). The major variation within adipose depots can be attributed to differences in the non-adipocyte component of adipose tissue. Using only non-obese subjects, we identified genes that were consistently differentially expressed between subcutaneous and omental adipose tissue, despite the variation in gene expression between these subjects. Using quantitative real time polymerase chain reaction (PCR), fatty acid binding protein 4 (FABP4), vimentin (Vim), four and a half LIMs domains (FHL1), CD36 (all higher in subcutaneous adipose tissue) and Matrix Gla protein (MGP; lower in subcutaneous adipose tissue) were confirmed to be significantly differentially expressed between depots.

CD36 Antigens↗
PubMed2005

Cholesterol regulation of genes involved in sterol trafficking in human THP-1 macrophages.

Modulation of the expression of genes involved in the control of cholesterol homeostasis by sterols in macrophages is crucial to foam cell formation. To characterize this regulation in THP-1 macrophages, we examined the effect of sterol loading and unloading on the expression of a number of genes that participate in lipoprotein uptake and cholesterol efflux. Sterol loading by exposure to acetylated LDL for 24 h resulted in an increase in free and esterified cholesterol of 1.4 and 1.8-fold, respectively. Under these conditions, the mRNA levels for SR-A were reduced a 59%, while those of CYP27 were increased by 4.6-fold. However, the expression of other genes involved in cholesterol efflux (ABCA1, ABCG1 and CLA-1) was not modified, despite a high intracellular cholesterol accumulation specially in the form of esterified cholesterol. On the other hand, HDL exposure reduced intracellular cholesterol content to 70%, and caused an increase in the expression of CD36 (78%), SR-A (51%) and CLA-1 (136%). Conversely, the expression of ABCA1, ABCG1 and CYP27 was decreased by 49, 67 and 57%, respectively. These findings indicate that in THP-1 macrophages, the expression of genes for receptors involved in lipoprotein binding and uptake tends to decrease upon cholesterol loading and to increase by cholesterol depletion, while the opposite pattern is found regarding the mRNA levels for proteins involved in cholesterol efflux.

ATP Binding Cassette Transporter 1↗
PubMed2006

Importance of LXR-alpha transcriptome in the modulation of innate immunity.

Liver-X-Receptor alpha (LXR-alpha) that belongs to nuclear receptor/transcriptional factor family has been recognized to play crucial role in the regulation of lipid metabolism and inflammation. Consequently, the present study was addressed to explore the functional genomics of LXR-alpha within human blood immunomodulatory cells. The results of such a study, which involved LXR-alpha gene silencing through siRNA approach, revealed that: (a) the mRNA expression of genes coding for IL-8, IL-4, CX3CR1, LDLR, hTERT and c-myc was significantly elevated in response to LXR-alpha gene silencing whereas mRNA expression of genes coding for PPARs(alpha, gamma), CD36 and Dicer could not be detected; (b) the expression of Receptor C( k ) protein remained unaffected; (c) the mRNA expression of IFN-gamma gene was down regulated in LXR-alpha knockdown cells. Based upon these results we propose that LXR-alpha gene plays a crucial role in the regulation of innate immunity at the genomic level.

CD36 Antigens↗
PubMed1995

Inhibitory effects of cerulenin on protein palmitoylation and insulin internalization in rat adipocytes.

Protein acylation by long-chain fatty acids has been suggested as a necessary step in membrane trafficking. Because several insulin effects are dependent upon membrane trafficking, the cellular effects of the protein acylation inhibitor cerulenin were examined. Cerulenin blocked palmitoylation of selected rat adipocyte proteins including CD36, the dominant marker for palmitoylation in adipocytes. To measure cerulenin's effects on insulin internalization, rat adipocytes were incubated with 125I-insulin at 37 degrees C in the presence or absence of cerulenin. Surface-bound and intracellular insulin were discriminated by the sensitivity of the former to rapid dissociation by a pH 3 buffer at 4 degrees C. Insulin internalization was inhibited 85% by 0.3 mM cerulenin. Inhibition required preincubation with the agent, was irreversible, was not dependent upon protein synthesis, and was not the result of ATP depletion. Cerulenin was also found to inhibit insulin-stimulated glucose uptake and acetyl-CoA carboxylase activity. Cerulenin had no effect on basal glucose uptake and utilization or on the uptake and retention of fatty acids. In summary, protein acylation may be an important step in insulin-regulated cellular functions dependent upon membrane trafficking, such as insulin internalization.

Acetyl-CoA Carboxylase↗
PubMed1991

Thrombospondin binds normally to glycoprotein IIIb deficient platelets.

Glycoprotein IIIb (GPIV, CD36) has been proposed as the platelet receptor for thrombospondin (TSP). We found two healthy blood donors, whose platelets were shown to be GPIIIb deficient. These platelets expressed endogeneous TSP as control platelets and their binding capacity for exogeneous TSP was the same. These results indicate that GPIIIb is not the major TSP receptor on platelets. However, it is not yet possible to exclude that in GPIIIb-deficient platelets other proteins may substitute for GPIIIb in TSP binding.

Adult↗
PubMed1995

Expression of the 85-kd membrane protein in primary human breast cancer: relationship to hormone receptor levels, DNA ploidy, and tumor grade.

Using the monoclonal antibody (MAb) MRK20 the immunohistochemical expression of the 85-kd membrane protein (MP)/cell adhesion molecule (CAM) CD36 was investigated in tumors from 41 patients with untreated breast adenocarcinoma. DNA ploidy as measured by flow cytometry and estrogen (ER) and progesterone receptor (PgR) tumor contents also were determined. Immunohistochemistry on frozen tissue showed expression of 85-kd MP localized to the carcinoma cells in tumors from 16 patients (39%). These samples also displayed variable staining of the capillary endothelium. Twenty-one samples (51%) showed 85-kd MP expression in small blood vessels. Thus, a total of 37 of 41 tumors (90%) were MAb MRK20 positive in carcinoma and/or mesenchymal cells. Expression of 85-kd MP in carcinoma cells was negatively associated with expression of ER (P < .05) and PgR (P < .01) receptors and positively associated with nondiploid tumors (P < 0.05) and tumor grade (P < .05). Axillary lymph node status, tumor size, and (patient) age were not associated with expression of 85-kd MP. In cytological smears obtained by fine-needle aspiration (FNA) cytology from 19 of the samples, expression of 85-kd MP in carcinoma cells showed a good correlation with tumor cell positivity in the corresponding histological section. Expression of 85-kd MP in breast carcinoma cells thus was associated with some recognized adverse prognostic factors. Future studies of its pathophysiological and prognostic roles in breast cancer seem warranted.

Adenocarcinoma↗
PubMed1995

Cloning the P. falciparum gene encoding PfEMP1, a malarial variant antigen and adherence receptor on the surface of parasitized human erythrocytes.

Plasmodium falciparum-infected human erythrocytes evade host immunity by expression of a cell-surface variant antigen and receptors for adherence to endothelial cells. These properties have been ascribed to P. falciparum erythrocyte membrane protein 1 (PfEMP1), an antigenically diverse malarial protein of 200-350 kDa on the surface of parasitized erythrocytes (PEs). We describe the cloning of two related PfEMP1 genes from the Malayan Camp (MC) parasite strain. Antibodies generated against recombinant protein fragments of the genes were specific for MC strain PfEMP1 protein. These antibodies reacted only with the surface of MC strain PEs and blocked adherence of these cells to CD36 but without effect on adherence to thrombospondin. Multiple forms of the PfEMP1 gene are apparent in MC parasites. The molecular basis for antigenic variation in malaria and adherence of infected erythrocytes to host cells can now be pursued.

Amino Acid Sequence↗
PubMed1990

Immunohistochemical comparison of actinic reticuloid with allergic contact dermatitis.

Biopsy specimens of chronic lesions and ultraviolet-induced lesions from actinic reticuloid patients were examined by immunoperoxidase techniques and compared with those of allergic contact dermatitis skin, one of the delayed-type hypersensitivity conditions. Each lesion of actinic reticuloid showed a clear predominance of suppressor/cytotoxic T cells to helper/inducer T cells and an increase of Langerhans cells in the epidermis and the dermis. These findings are generally similar to those in the late phase (on day 7 and 11) but not in the early phase (on day 2) of allergic contact dermatitis and suggest that delayed-type hypersensitivity might be involved in some parts of the pathogenesis of actinic reticuloid. CD36+DR+ epidermal cells were also observed in ultraviolet-induced lesions from actinic reticuloid patients, suggesting a possible role in the modulation of the mechanism.

Aged↗
PubMed2006

The effect of tocopheryl phosphates on atherosclerosis progression in rabbits fed with a high cholesterol diet.

The effect of tocopheryl phosphate on atherosclerosis progression has been studied in rabbits, fed with a 2% cholesterol diet and compared with an equivalent amount of alpha-tocopheryl acetate. The results show that the atherosclerotic-preventing effect of the phosphate derivative was more pronounced than that of the acetate derivative. alpha-Tocopheryl phosphate was also more potent in diminishing the expression of CD36 than the acetate derivative.

Animals↗
PubMed2005

Macrophage foam-cell formation in streptozotocin-induced diabetic mice: stimulatory effect of glucose.

BACKGROUND: Diabetes is associated with an increased risk for atherosclerosis. We investigated the effect of diabetes induction on atherogenesis and on macrophage-foam cell formation. METHODS AND RESULTS: Atherosclerotic apolipoprotein-E-deficient mice were converted into diabetic mice by streptozotocin injection. Aortic atherosclerotic lesion area was significantly enhanced by 67% and 106% in mice that were diabetic for 1 and 3 months, respectively, compared to the non-diabetic mice. Moreover, mouse peritoneal macrophages (MPM) from diabetic mice for 1 and 3 months exhibit higher lipid peroxides content by 55% and 63%, respectively, in association with the MPM glucose content. Oxidized LDL (Ox-LDL) uptake by MPM obtained from diabetic mice for 1 and 3 months was significantly increased by 36% and 45%, respectively, in association with the increased macrophage cholesterol content. To determine whether the accelerated foam cell formation in diabetic mice could result from a direct effect of glucose on macrophages, J-774-A.1 macrophages were incubated with increasing glucose concentrations (2.5-62 mM). Glucose-enriched macrophages exhibit dose-dependent higher peroxides content up to 7.5-fold and increased Ox-LDL cellular uptake associated with up-regulation of the scavenger receptor CD36 at the mRNA level. CONCLUSION: Induction of diabetes in atherosclerotic mice led to an accelerated atherosclerosis and macrophage-derived foam cell formation, probably by involving a glucose-dependent related mechanism.

Animals↗
PubMed2004

Identification of hepatic molecular mechanisms of action of alpha-tocopherol using global gene expression profile analysis in rats.

The recent discovery that vitamin E (VE) regulates gene activity at the transcriptional level indicates that VE may exert part of its biological effects by mechanisms which may be independent of its well-recognised antioxidant function. The objective of this study was the identification of hepatic vitamin E-sensitive genes and examination of the effects of VE on their corresponding biological endpoints. Two groups of male rats were randomly assigned to either a VE-sufficient diet or to a control diet deficient in VE for 290 days. High-density oligonucleotide microarrays comprising over 7000 genes were used to assess the transcriptional response of the liver. Differential gene expression was monitored over a period of 9 months, at four different time-points, and rats were individually profiled. This experimental strategy identified several VE-sensitive genes, which were chronically altered by dietary VE. VE supplementation down-regulated scavenger receptor CD36, coagulation factor IX and 5-alpha-steroid reductase type 1 mRNA levels while hepatic gamma glutamyl-cysteinyl synthetase was significantly up-regulated. Measurement of the corresponding biological endpoints such as activated partial thromboplastin time, plasma dihydrotestosterone and hepatic glutathione substantiated the gene chip data which indicated that dietary VE plays an important role in a range of metabolic processes within the liver.

Animal Feed↗
PubMed2004

Gene expression profiling identifies retinoids as potent inducers of macrophage lipid efflux.

Vitamin A and its naturally occurring derivatives 9-cis retinoic acid (9-cis RA) and all-trans retinoic acid (ATRA) exert a variety of biological effects including immunomodulation, growth, differentiation, and apoptosis of normal and neoblastic cells. In order to directly study the effects of these retinoids on macrophage gene expression and lipid metabolism, primary human monocytes and in vitro differentiated macrophages were stimulated with beta-carotene, 9-cis RA, and ATRA and global gene expression profiles were analyzed by Affymetrix DNA-microarrays and differentially regulated genes were verified by quantitative TaqMan RT-PCR. Among others, we have identified a strong up-regulation of a cluster of genes involved in cholesterol metabolism including apolipoproteins (apoC-I, apoC-II, apoC-IV, apoE), the scavenger receptor CD36, steroid-27-hydroxylase (CYP27A1), liver X receptor alpha (LXRalpha), and ATP-binding cassette transporters A1 (ABCA1) and G1 (ABCG1). Since the CYP27A1 gene displayed the strongest up-regulation on the mRNA level, we cloned various deletion constructs of the promoter region and analyzed the response to retinoids in macrophages. Thereby, a novel retinoic acid-responsive element could be located within 191 bp of the proximal CYP27A1 promoter. To further assess the functional consequences of retinoid receptor action, we carried out phospholipid and cholesterol efflux assays. We observed a strong induction of apoA-I-dependent lipid efflux in stimulated macrophages, implicating an important role for retinoids in cellular functions of macrophages.

ATP-Binding Cassette Transporters↗
PubMed2005

Exercise might favor reverse cholesterol transport and lipoprotein clearance: potential mechanism for its anti-atherosclerotic effects.

Livers of C57 BL/6 mice exercised for 2 weeks showed a dramatic increase in scavenger receptor B1 (SR-B1), CD36 and low density lipoprotein (LDL) receptor and a decrease in acetyl LDL receptor gene expression. These effects on lipoprotein receptors are reminiscent of the effects mediated by peroxisome proliferator-activated receptor (PPARgamma) ligands.

Animals↗
PubMed2004

Modulation of cell proliferation and gene expression by alpha-tocopheryl phosphates: relevance to atherosclerosis and inflammation.

The effect of a mixture of alpha-tocopheryl phosphate and di-alpha-tocopheryl phosphate (TPm) was studied in vitro on two cell lines, RASMC (from rat aortic smooth muscle) and human THP-1 monocytic leukaemia cells. Inhibition of cell proliferation by TPm was shown in both lines and occurred with TPm at concentrations lower than those at which alpha-tocopherol was equally inhibitory. TPm led in non-stimulated THP-1 cells to inhibition of CD36 mRNA and protein expression, to inhibition of oxidized low density lipoprotein surface binding and oxLDL uptake. In non-stimulated THP-1 cells, alpha-tocopherol had only very weak effects on these events. Contrary to alpha-tocopherol, TPm was cytotoxic to THP-1 cells at high concentrations. Thus, TPm is able to inhibit the major aggravating elements involved in the progression of atherosclerosis. The higher potency of TPm may be due to a better uptake of the molecule and to its intracellular hydrolysis, providing more alpha-tocopherol to sensitive sites. Alternatively, a direct effect of the phosphate ester on specific cell targets may be considered.

Animals↗
PubMed2006

Oxidative stress influences cholesterol efflux in THP-1 macrophages: role of ATP-binding cassette A1 and nuclear factors.

OBJECTIVES: Understanding the mechanisms involved in oxidative stress-induced foam cell formation is of fundamental importance for atherosclerosis. Our aim was to characterize the effects of oxidative stress on key receptors of macrophage cholesterol homeostasis, on the nuclear transcription factors PPAR and LXR regulating their expression, and on macrophage cholesterol handling. METHODS AND RESULTS: The incubation of macrophages derived from the human monocyte cell line THP-1 with iron (100 microm)/ascorbate (1000 microm) for a period of 4 h induced a strong peroxidation, as demonstrated by the elevation of malondialdehyde (220%, P < 0.001). The production of lipid peroxidation affected cholesterol efflux, which was probably due to decreased ABCAI gene and protein expression. On the other hand, cholesterol influx remained unchanged as did the mRNA and protein levels of SR-BI and CD36, important protein receptors that participate in cholesterol import. Experiments using RT-PCR showed that the ABCAI modulation was orchestrated by the nuclear receptors LXRalpha, LXRbeta, PPARalpha, and PPARgamma. Treatment with powerful antioxidants (Trolox and BHT) prevented the adverse effects of iron-ascorbate on cholesterol movement, conceivably supporting the role of oxidative stress. CONCLUSION: Our results show that oxidative stress can directly be induced in macrophages and concomitantly impairs the expression of receptors involved in cholesterol flux, which could influence foam cell formation and atherosclerosis development.

ATP Binding Cassette Transporter 1↗
PubMed2005

The human placental derived BeWo cell line: a useful model for selecting Plasmodium falciparum CSA-binding parasites.

Chondroitin sulfate A (CSA) present in the placental intervillous blood spaces has been described as the main receptor involved in the massive sequestration of Plasmodium falciparum parasitized erythrocytes to the placenta. Placental parasite isolates are functionally distinct from isolates that sequester in other organs, because they do not cytoadhere to CD36 but instead bind to CSA. To investigate for the parasites molecules associated with the CSA adhesion phenotype, different methodologies have been developed to select for CSA-binding lines in vitro mainly using non-placental sources of CSA that differ in their sulfation pattern. In this study, we show that the human trophoblastic BeWo cell line is a very efficient alternative to select for the CSA-binding phenotype in parasitized erythrocytes.

Animals↗