Article

Pathophysiology of human genetic CD36 deficiency.

Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Suita, Japan.
Trends in Cardiovascular Medicine (impact factor: 2.49). 06/2003; 13(4):136-41. pp.136-41
Source: PubMed

ABSTRACT CD36, originally identified as glycoprotein IV on platelets, is an 88-kDa integral membrane protein that has multiple ligands and is expressed in the cardiovascular system (ie, blood vessel walls and the heart). Human genetic CD36 deficiency is relatively frequent in Asian and African populations. Investigation into the pathophysiology of this disorder has shown that CD36 may play an important role as a major scavenger receptor for oxidized low-density lipoproteins and as a crucial transporter for long-chain fatty acids. The CD36 deficiency may be related to the phenotypic expression of the "metabolic syndrome," which is frequently associated with atherosclerotic cardiovascular diseases. It also has been reported that CD36 deficiency might be linked with cardiomyopathy. These data raised the possibility that CD36 deficiency might be an important genetic background for these life-threatening human cardiovascular diseases.

0 0
 · 
0 Bookmarks
 · 
27 Views
  • Source
    Article: Single-nucleotide polymorphism of CD36 locus and obesity in European adolescents.
    Szilvia Bokor, Vanessa Legry, Aline Meirhaeghe, Jonatan R Ruiz, Beatrice Mauro, Kurt Widhalm, Yannis Manios, Philippe Amouyel, Luis A Moreno, Dènes Molnàr, Jean Dallongeville
    [show abstract] [hide abstract]
    ABSTRACT: CD36 is a membrane receptor with a wide variety of functions, including the regulation of energy metabolism, fat storage, and adipocyte differentiation. To assess the relationship between CD36 gene single-nucleotide polymorphisms (SNPs) and obesity in adolescents, we evaluated the relationship between CD36 SNPs and the risk of obesity in a case-control study composed of 307 obese (age = 15.0 +/- 1.1 years) and 339 normal-weight adolescents (age = 14.6 +/- 1.1 years). To validate the results, we assessed the relation between the same SNPs and percentage of body fat (BF%) and BMI in 1,151 European adolescents (age = 14.8 +/- 1.4 years). SNPs with a minor allele frequency >0.10 were selected to tag CD36. Genotyping was performed on an Illumina system. Four SNPs (rs3211867, rs3211883, rs3211908, and rs1527483) were associated with increased risk of obesity in the case-control study (odds ratio (OR) (95% confidence interval)): 1.96 (1.26-3.04], P = 0.003; 1.73 (1.16-2.59), P = 0.007; 2.42 (1.47-4.01), P = 0.0005 and 1.95 (1.25-3.05), P = 0.003, respectively). The same four SNPs were associated with higher BMI (P < 0.05) and BF% (P < 0.04) in the validation study. Further analyses identified a haplotype (frequency: 0.05) carrying the minor allele of these SNPs as being associated with obesity (OR: 2.28; P = 0.0008) in the case-control study and with excess adiposity (i.e., higher BF% (P = 0.03) and BMI (P = 0.04)) in the validation study. Our data suggest that genetic variability at the CD36 gene locus could be associated with body weight variability in European adolescents but these findings require replication.
    Obesity 11/2009; 18(7):1398-403. · 4.28 Impact Factor
  • Source
    Article: Comparison of gene expression profiles between human and mouse monocyte subsets.
    Molly A Ingersoll, Rainer Spanbroek, Claudio Lottaz, Emmanuel L Gautier, Marion Frankenberger, Reinhard Hoffmann, Roland Lang, Muzlifah Haniffa, Matthew Collin, Frank Tacke, Andreas J R Habenicht, Loems Ziegler-Heitbrock, Gwendalyn J Randolph
    [show abstract] [hide abstract]
    ABSTRACT: Blood of both humans and mice contains 2 main monocyte subsets. Here, we investigated the extent of their similarity using a microarray approach. Approximately 270 genes in humans and 550 genes in mice were differentially expressed between subsets by 2-fold or more. More than 130 of these gene expression differences were conserved between mouse and human monocyte subsets. We confirmed numerous of these differences at the cell surface protein level. Despite overall conservation, some molecules were conversely expressed between the 2 species' subsets, including CD36, CD9, and TREM-1. Other differences included a prominent peroxisome proliferator-activated receptor gamma (PPARgamma) signature in mouse monocytes, which is absent in humans, and strikingly opposed patterns of receptors involved in uptake of apoptotic cells and other phagocytic cargo between human and mouse monocyte subsets. Thus, whereas human and mouse monocyte subsets are far more broadly conserved than currently recognized, important differences between the species deserve consideration when models of human disease are studied in mice.
    Blood 12/2009; 115(3):e10-9. · 9.90 Impact Factor
  • Source
    Article: Role of fatty acid transporters in epidermis: Implications for health and disease.
    Denis Khnykin, Jeffrey H Miner, Frode Jahnsen
    [show abstract] [hide abstract]
    ABSTRACT: Skin epidermis is an active site of lipid synthesis. The intercellular lipids of human stratum corneum (SC) are unique in composition and quite different from the lipids found in most biological membranes. The three major lipids in the SC are free fatty acids, cholesterol and ceramides. Fatty acids can be synthesized by keratinocytes de novo and, in addition, need to be taken up from the circulation. The latter process has been shown to be protein mediated, and several fatty acid transporters are expressed in skin. Recent studies of transgenic and knockout animal models for fatty acid transporters and the identification of fatty acid transport protein 4 (FATP4 or SLC27A4) mutations as causative for Ichthyosis Prematurity Syndrome highlight the vital roles of fatty acid transport and metabolism in skin homeostasis. This review provides an overview of our current understanding of the role of fatty acids and their transporters in cutaneous biology, including their involvement in epidermal barrier generation and skin inflammation.
    Dermato-endocrinology. 04/2011; 3(2):53-61.

Show more

Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.

Keywords

African populations
 
atherosclerotic cardiovascular diseases
 
blood vessel walls
 
cardiovascular system
 
CD36 deficiency
 
crucial transporter
 
Human genetic CD36 deficiency
 
life-threatening human cardiovascular diseases
 
major scavenger receptor
 
oxidized low-density lipoproteins
 
phenotypic expression
 
platelets
 

Ken-ichi Hirano