Influence of CD36 Deficiency on Heart Disease in Children

Teraguchi, Masayuki; Ikemoto, Yumiko; Unishi, Gen; Ohkohchi, Hiroyuki; Kobayashi, Yohnosuke

doi:10.1253/circj.68.435

Cited by 8 publications

(4 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Of note, clinical study shows that high serum ox-LDL level remarkably correlates with total fructose intake in children with non-alcoholic fatty liver disease at baseline, and it is significantly reduced after low-fructose diet education for six months 7 . Patients with CD36 deficiency may be susceptible to myocardial damage with abnormal myocardial long-chain fatty acid metabolism 50 . TXNIP up-regulation is observed in cardiomyocyte impairment of diabetic mice 15 , and closely correlates with oxidative stress initiated by CD36 in ceramide-induced pancreatic β-cell dysfunction 17 .…”

Section: Discussionmentioning

confidence: 99%

Cinnamaldehyde and allopurinol reduce fructose-induced cardiac inflammation and fibrosis by attenuating CD36-mediated TLR4/6-IRAK4/1 signaling to suppress NLRP3 inflammasome activation

Kang

Zhang

et al. 2016

Sci Rep

View full text Add to dashboard Cite

Fructose consumption induces metabolic syndrome to increase cardiovascular disease risk. Cinnamaldehyde and allopurinol possess anti-oxidative and anti-inflammatory activity to relieve heart injury in metabolic syndrome. But the mechanisms of fructose-induced cardiac injury, and cardioprotective effects of cinnamaldehyde and allopurinol are not completely understood. In this study, fructose-fed rats displayed metabolic syndrome with elevated serum ox-LDL, cardiac oxidative stress, inflammation and fibrosis. Scavenger receptor CD36, Toll-like receptor 4 (TLR4), TLR6, IL-1R-associated kinase 4/1 (IRAK4/1), nucleotide-binding domain (NOD)-like receptor protein 3 (NLRP3) inflammasome, interleukin-1β, transforming growth factor-β (TGF-β), drosophila mothers against DPP homolog (Smad) 2/3 phosphorylation and Smad4 were increased in animal and H9c2 cell models. These pathological processes were further evaluated in ox-LDL or fructose-exposed H9c2 cells pretreated with ROS scavenger and CD36 specific inhibitor, or IRAK1/4 inhibitor, and transfected with CD36, NLRP3, or IRAK4/1 siRNA, demonstrating that NLPR3 inflammasome activation through CD36-mediated TLR4/6-IRAK4/1 signaling may promote cardiac inflammation and fibrosis. Cinnamaldehyde and allopurinol reduced cardiac oxidative stress to suppress NLPR3 inflammasome activation and TGF-β/Smads signaling by inhibiting CD36-mediated TLR4/6-IRAK4/1 signaling under fructose induction. These results suggest that the blockage of CD36-mediated TLR4/6-IRAK4/1 signaling to suppress NLRP3 inflammasome activation by cinnamaldehyde and allopurinol may protect against fructose-induced cardiac inflammation and fibrosis.

show abstract

Section: Discussionmentioning

confidence: 99%

Cinnamaldehyde and allopurinol reduce fructose-induced cardiac inflammation and fibrosis by attenuating CD36-mediated TLR4/6-IRAK4/1 signaling to suppress NLRP3 inflammasome activation

Kang

Zhang

et al. 2016

Sci Rep

View full text Add to dashboard Cite

show abstract

“…Patients with type II CD36 deficiency have normal platelet functions, 76 while the incidence of cardiomyopathy, hyperlipidemia and insulin resistance are relatively high in these patients. 77, 78, 79, 80 It is not clear if the effects of human CD36 deficiency are caused by the lack of CD36 in certain cell types or if there are aberrant functions of mutant CD36 or any compensatory effects. Therefore, additional studies are warranted to clarify the effects of CD36 deficiency in humans.…”

Section: Genetic Variations Of Cd36mentioning

confidence: 99%

CD36, a scavenger receptor implicated in atherosclerosis

2014

View full text Add to dashboard Cite

CD36 is a membrane glycoprotein that is present on various types of cells, including monocytes, macrophages, microvascular endothelial cells, adipocytes and platelets. Macrophage CD36 participates in atherosclerotic arterial lesion formation through its interaction with oxidized low-density lipoprotein (oxLDL), which triggers signaling cascades for inflammatory responses. CD36 functions in oxLDL uptake and foam cell formation, which is the initial critical stage of atherosclerosis. In addition, oxLDL via CD36 inhibits macrophage migration, which may be a macrophage-trapping mechanism in atherosclerotic lesions. The role of CD36 was examined in in vitro studies and in vivo experiments, which investigated various functions of CD36 in atherosclerosis and revealed that CD36 deficiency reduces atherosclerotic lesion formation. Platelet CD36 also promotes atherosclerotic inflammatory processes and is involved in thrombus formation after atherosclerotic plaque rupture. Because CD36 is an essential component of atherosclerosis, defining the function of CD36 and its corresponding signaling pathway may lead to a new treatment strategy for atherosclerosis.

show abstract

“…Quantitative analysis of monocyte CD36 surface expression is of potential interest in a variety of clinical and research settings including malaria (8), metabolic disorders from dyslipidemia (5) to diabetes, (6,10) and ischemic (11) or hypertrophic (12,13) cardiomyopathy. Because a forward scatter threshold is commonly used to eliminate small particles including non-adherent platelets from flow cytometric analysis, the effect of platelet concentration on monocyte CD36 fluorescence is easily overlooked.…”

Section: Discussionmentioning

confidence: 99%

When monocytes and platelets compete: The effect of platelet count on the flow cytometric measurement of monocyte CD36

Dzik

Cserti‐Gazdewich

Ssewanyana

et al. 2009

Cytometry Part B Clinical

View full text Add to dashboard Cite

Background: Flow cytometric measurement of monocyte surface CD36 is relevant to several conditions including diabetes, cardiovascular disease, lipid disorders, platelet isoimmunization, and susceptibility to P falciparum malaria. CD36 is also strongly expressed on platelets where it is also known as platelet glycoprotein IV.Methods: Whole blood samples, containing identical monocyte concentrations, were adjusted to contain platelets ranging from 20,000/uL to 600,000/uL, were stained with fluorescent-labeled anti-CD36, and analyzed by flow cytometry.Results: CD36 median fluorescent intensity (MFI) observed on monocytes decreased as the platelet concentration in the sample increased with more than a 50% decline in monocyte MFI over the normal range of platelet values. The effect was not abolished by using larger volumes of monoclonal antibody and was observed with different clones of reagent anti-CD36. The findings were most consistent with competition by platelets for the CD36 reagent. Similar findings were observed with antibody to class I HLA. Under defined assay conditions, monocyte CD36 MFI declined with rising platelet concentration in a predictable fashion following an inverse linear relationship.Conclusions: Measurement of CD36 expression on monocytes by flow cytometry in whole blood samples is affected by the sample platelet count. When comparing the monocyte CD36 expression among different individuals, our approach can be used to adjust measured monocyte CD36 expression for the effect of the platelet concentration in the sample. Competition by platelets for monoclonal reagents may occur in other settings when whole blood assays are used and when the target antigen is strongly expressed on both platelets and leukocytes.

show abstract

Influence of CD36 Deficiency on Heart Disease in Children

Cited by 8 publications

References 22 publications

Cinnamaldehyde and allopurinol reduce fructose-induced cardiac inflammation and fibrosis by attenuating CD36-mediated TLR4/6-IRAK4/1 signaling to suppress NLRP3 inflammasome activation

Cinnamaldehyde and allopurinol reduce fructose-induced cardiac inflammation and fibrosis by attenuating CD36-mediated TLR4/6-IRAK4/1 signaling to suppress NLRP3 inflammasome activation

CD36, a scavenger receptor implicated in atherosclerosis

When monocytes and platelets compete: The effect of platelet count on the flow cytometric measurement of monocyte CD36

Contact Info

Product

Resources

About