Molecular Basis of Human CD36 Gene Mutations

Rać, Monika; Safranow, Krzysztof; Poncyljusz, Wojciech

doi:10.2119/2006-00088.rac

Cited by 103 publications

(44 citation statements)

References 92 publications

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“…CD36 gene deficiency is much more prevalent in Asian populations than in Caucasians (0%–0.3%) (Tanaka et al., 2001). This deficiency causes platelet refractoriness, post-transfusion thrombocytopenic purpura, neonatal alloimmune thrombocytopenia, and other disorders (Hirano et al., 2003, Neculai et al., 2013, Rac et al., 2007). However, deficiency of CD36 has no effect on development of erythroblasts (Toba et al., 2001).…”

Section: Discussionmentioning

confidence: 99%

Early Development of Definitive Erythroblasts from Human Pluripotent Stem Cells Defined by Expression of Glycophorin A/CD235a, CD34, and CD36

Mao

Huang

et al. 2016

Stem Cell Reports

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SummaryThe development of human erythroid cells has been mostly examined in models of adult hematopoiesis, while their early derivation during embryonic and fetal stages is largely unknown. We observed the development and maturation of erythroblasts derived from human pluripotent stem cells (hPSCs) by an efficient co-culture system. These hPSC-derived early erythroblasts initially showed definitive characteristics with a glycophorin A+ (GPA+) CD34lowCD36− phenotype and were distinct from adult CD34+ cell-derived ones. After losing CD34 expression, early GPA+CD36− erythroblasts matured into GPA+CD36low/+ stage as the latter expressed higher levels of β-globin along with a gradual loss of mesodermal and endothelial properties, and terminally suppressed CD36. We establish a unique in vitro model to trace the early development of hPSC-derived erythroblasts by serial expression of CD34, GPA, and CD36. Our findings may provide insight into the understanding of human early erythropoiesis and, ultimately, therapeutic potential.

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Section: Discussionmentioning

confidence: 99%

Early Development of Definitive Erythroblasts from Human Pluripotent Stem Cells Defined by Expression of Glycophorin A/CD235a, CD34, and CD36

Mao

Huang

et al. 2016

Stem Cell Reports

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“…The functions of CD36 include removal of oxidized LDL (oxLDL) and fatty acid from plasma by macrophages and monocytes (Park et al 2009; Rać et al 2007), induction of apoptosis (Silverstein 2009), and enhancement of cytoadherence of abnormally shaped erythrocytes (Chilongola et al 2009). …”

Section: Introductionmentioning

confidence: 99%

Polymorphism of the CD36 Gene and Cardiovascular Risk Factors in Patients with Coronary Artery Disease Manifested at a Young Age

et al. 2011

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This study investigates potential associations between CD36 gene variants and the presence of risk factors in Caucasians with coronary artery disease (CAD) manifested at a young age. The study group consisted of 90 patients; the men were ≤ 50 years old and the women were ≤ 55 years old. Amplicons of exons 4 and 5 including fragments of introns were analyzed by DHPLC. Two polymorphisms were found: IVS3-6 T/C (rs3173798) and IVS4-10 G/A (rs3211892). The C allele of the IVS3-6 T/C polymorphism was associated with higher prevalence of obesity and diabetes, higher hsCRP, lower Lp(a) serum concentrations, and younger age at myocardial infarction. The A allele of the IVS4-10 G/A polymorphism was associated with older age of myocardial infarction and higher white blood cell count. The functional role of CD36 polymorphisms in CAD development needs further research.

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“…It plays a key role in fatty acid and glucose metabolism, and its dysregulation is involved in glucose intolerance and diabetes (Hajri et al 2002, Rac et al 2007.…”

Section: Discussionmentioning

confidence: 99%

Bisphenol A effects on gene expression in adipocytes from children: association with metabolic disorders

Menale¹,

Piccolo²,

Cirillo³

et al. 2015

Journal of Molecular Endocrinology

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Bisphenol A (BPA) is a xenobiotic endocrine-disrupting chemical. In vitro and in vivo studies have indicated that BPA alters endocrine-metabolic pathways in adipose tissue, which increases the risk of metabolic disorders and obesity. BPA can affect adipose tissue and increase fat cell numbers or sizes by regulating the expression of the genes that are directly involved in metabolic homeostasis and obesity. Several studies performed in animal models have accounted for an obesogen role of BPA, but its effects on human adipocytesespecially in children -have been poorly investigated. The aim of this study is to understand the molecular mechanisms by which environmentally relevant doses of BPA can interfere with the canonical endocrine function that regulates metabolism in mature human adipocytes from prepubertal, non-obese children. BPA can act as an estrogen agonist or antagonist depending on the physiological context. To identify the molecular signatures associated with metabolism, transcriptional modifications of mature adipocytes from prepubertal children exposed to estrogen were evaluated by means of microarray analysis. The analysis of deregulated genes associated with metabolic disorders allowed us to identify a small group of genes that are expressed in an opposite manner from that of adipocytes treated with BPA. In particular, we found that BPA increases the expression of pro-inflammatory cytokines and the expression of FABP4 and CD36, two genes involved in lipid metabolism. In addition, BPA decreases the expression of PCSK1, a gene involved in insulin production. These results indicate that exposure to BPA may be an important risk factor for developing metabolic disorders that are involved in childhood metabolism dysregulation.

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Molecular Basis of Human CD36 Gene Mutations

Cited by 103 publications

References 92 publications

Early Development of Definitive Erythroblasts from Human Pluripotent Stem Cells Defined by Expression of Glycophorin A/CD235a, CD34, and CD36

Early Development of Definitive Erythroblasts from Human Pluripotent Stem Cells Defined by Expression of Glycophorin A/CD235a, CD34, and CD36

Polymorphism of the CD36 Gene and Cardiovascular Risk Factors in Patients with Coronary Artery Disease Manifested at a Young Age

Bisphenol A effects on gene expression in adipocytes from children: association with metabolic disorders

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