Endothelin-1 decreases CD36 protein expression in vascular smooth muscle cells

Kwok, Ching Fai; Juan, Chi Chang; Ho, Low Tone

doi:10.1152/ajpendo.00084.2006

Cited by 19 publications

(17 citation statements)

References 44 publications

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“…The reduced level of CD36 on SAD RBC could result from the high plasma level of endothelin-1 found in both SS patients and SAD mice, 34,35 which decreases CD36 protein expression, an effect recently reported for vascular smooth muscle cells. 36 In conclusion, the present work shows an over-adhesiveness to endothelium of SAD mouse RBC, with this phenomenon depending on two adhesion proteins, ICAM-4 and CD36, as previously reported for human SS RBC. Thus, the transgenic SAD mouse could serve as a useful model for investigating the individual contributions of the different erythrocyte and endothelial adhesion molecules to vaso-occlusive events, and for evaluating the therapeutic efficacy of blocking peptides or monoclonal antibodies.…”

Section: Discussionsupporting

confidence: 88%

Intercellular adhesion molecule-4 and CD36 are implicated in the abnormal adhesiveness of sickle cell SAD mouse erythrocytes to endothelium

Trinh–Trang–Tan¹,

Vilela-Lamego²,

Picot³

et al. 2009

Haematologica

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BackgroundAbnormal adhesiveness of red blood cells to endothelium has been implicated in vaso-occlusive crisis of sickle cell disease. The present study examined whether the SAD mouse model exhibits the same abnormalities of red blood cell adhesion as those found in human sickle cell disease. Design and MethodsThe repertoire of adhesive molecules on murine erythrocytes and bEnd.3 microvascular endothelial cells was determined by flow cytometry using monoclonal antibodies or by western blotting. Adhesion was investigated in dynamic conditions and measured at different shear stresses. ResultsCD36, CD47 and intercellular adhesion molecular-4, but not Lutheran blood group antigen/basal cell adhesion molecule, are present on mouse mature erythrocytes. a4β1 are not expressed on SAD and wild type reticulocytes. Endothelial bEnd.3 cells express aVβ3, a4β1, CD47, vascular cell adhesion molecule-1, and Lutheran blood group antigen/basal cell adhesion molecule, but not CD36. Adhesion of SAD red cells is: (i) 2-to 3-fold higher than that of wild type red cells; (ii) further increased on platelet activating factor-activated endothelium; (iii) not stimulated by epinephrine; (iv) inhibited after treating the endothelium with a peptide reproducing one of the binding sequences of mouse intercellular adhesion molecular-4, or with monoclonal antibody against murine av integrin; and (v) inhibited after pretreatment of red blood cells with anti-mouse CD36 monoclonal antibodies. The combination of treatments with intercellular adhesion molecular-4 peptide and anti-CD36 monoclonal antibodies eliminates excess adhesion of SAD red cells. The phosphorylation state of intercellular adhesion molecular-4 and CD36 is probably not involved in the over-adhesiveness of SAD erythrocytes. ConclusionsIntercellular adhesion molecular-4/avβ3 and CD36/thrombospondin interactions might contribute to the abnormally high adhesiveness of SAD red cells. The SAD mouse is a valuable animal model for investigating adhesion processes of sickle cell disease. Haematologica 2010;95:730-737. doi:10.3324/haematol.2009 Intercellular adhesion molecule-4 and CD36 are implicated in the abnormal adhesiveness of sickle cell SAD mouse erythrocytes to endothelium © F e r r a t a S t o r t i F o u n d a t i o n

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Section: Discussionsupporting

confidence: 88%

Intercellular adhesion molecule-4 and CD36 are implicated in the abnormal adhesiveness of sickle cell SAD mouse erythrocytes to endothelium

Trinh–Trang–Tan¹,

Vilela-Lamego²,

Picot³

et al. 2009

Haematologica

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“…CD64, or FcgRIA, mediates receptor-mediated endocytosis of IgG-antigen complexes in macrophages (27). CD36, a scavenger receptor, mediates macrophage uptake of oxidized low-density lipoprotein, as well as serving as a surface receptor for thrombospondin-1 (28)(29)(30). CD163 serves as a macrophage cell surface hemoglobin scavenger receptor and was recently shown to be highly predictive of mortality in pneumococcal bacteremia (24,31).…”

Section: Discussionmentioning

confidence: 99%

Circulating RNA Transcripts Identify Therapeutic Response in Cystic Fibrosis Lung Disease

Saavedra¹,

Hughes²,

Sanders³

et al. 2008

Am J Respir Crit Care Med

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Rationale: Circulating leukocyte RNA transcripts are systemic markers of inflammation, which have not been studied in cystic fibrosis (CF) lung disease. Although the standard assessment of pulmonary treatment response is FEV 1 , a measure of airflow limitation, the lack of systemic markers to reflect changes in lung inflammation critically limits the testing of proposed therapeutics. Objectives: We sought to prospectively identify and validate peripheral blood leukocyte genes that could mark resolution of pulmonary infection and inflammation using a model by which RNA transcripts could increase the predictive value of spirometry. Methods: Peripheral blood mononuclear cells were isolated from 10 patients with CF and acute pulmonary exacerbations before and after therapy. RNA expression profiling revealed that 10 genes significantly changed with treatment when compared with matched non-CF and control subjects with stable CF to establish baseline transcript abundance. Peripheral blood mononuclear cell RNA transcripts were prospectively validated, using real-time polymerase chain reaction amplification, in an independent cohort of acutely ill patients with CF (n 5 14). Patients who responded to therapy were analyzed using general estimating equations and multiple logistic regression, such that changes in FEV 1 % predicted were regressed with transcript changes. Measurements and Main Results: Three genes, CD64, ADAM9, and CD36, were significant and independent predictors of a therapeutic response beyond that of FEV 1 alone (P , 0.05). In both cohorts, receiver operating characteristic analysis revealed greater accuracy when genes were combined with FEV 1 . Conclusions: Circulating mononuclear cell transcripts characterize a response to the treatment of pulmonary exacerbations. Even in small patient cohorts, changes in gene expression in conjunction with FEV 1 may enhance current outcomes measures for treatment response.

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“…These studies, while showing a critical role for platelet CD36 in thrombosis, do not rule out a role for CD36-mediated signaling in other vascular cells in promoting thrombosis. Although CD36 is not expressed on large-vessel endothelial cells (5,6), several groups have reported that VSMCs in culture express low levels of CD36 (7)(8)(9)(10)(11)(12) and that expression can be upregulated by PPARγ (9). No function for CD36 has been identified, however, on VSMCs.…”

Section: Introductionmentioning

confidence: 99%

CD36 participates in a signaling pathway that regulates ROS formation in murine VSMCs

et al. 2010

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CD36 is a membrane glycoprotein expressed on platelets, monocytes, macrophages, and several other cell types that was recently demonstrated to be involved in platelet activation in response to oxidized phospholipids, including oxidized LDL. Although the role of CD36 in other vascular cells has not been well defined, previous studies have demonstrated that cd36-knockout (cd36 -/-) mice have prolonged thrombosis times after vascular injury, which can be protective in the state of hyperlipidemia. Here, we found significantly less ROS in the vessel walls of cd36 -/-mice compared with WT after chemically induced arterial injury, suggesting that CD36 may contribute to ROS generation in the VSMCs themselves. Gene expression analysis revealed that the antioxidant enzymes peroxiredoxin-2 (Prdx2) and heme oxygenase-1 were upregulated in cd36 -/-VSMCs. Molecular dissection of the pathway in isolated mouse VSMCs revealed CD36 ligand-dependent induction of Fyn phosphorylation, with subsequent phosphorylation and degradation of the redox-sensitive transcription factor Nrf2. Chromatin immunoprecipitation experiments further showed that Nrf2 directly occupied the Prdx2 promoter. The importance of this pathway was evidenced by increased ROS generation in prdx2 -/-mice and decreased thrombosis times in both prdx2 -/-and nrf2 -/-mice after vascular injury. These data suggest that CD36-mediated downregulation of antioxidant systems in VSMCs may contribute to its prothrombotic, proinflammatory, and atherogenic effects. Introduction CD36, a class B scavenger receptor, is an 88-kDa membrane glycoprotein expressed on platelets, monocytes, macrophages, and several other cell types (1). It is a multifunctional receptor with independent capacity to bind 3 major classes of ligands: modified phospholipids, long-chain fatty acids, and proteins containing thrombospondin structural homology domains. Although CD36 was first identified on platelets, its role in platelet function remained undefined until recently, when our group showed that CD36 promotes platelet activation in response to oxidized phospholipids, including oxidized LDL (oxLDL) (2). We found that genetic deletion of CD36 in mice protected them from the prothrombotic state associated with hyperlipidemia (2) and oxidant stress and also significantly prolonged thrombotic occlusion times after vascular injury induced by ferric chloride (FeCl 3 ) (3). The mechanisms underlying this phenotype remain incompletely understood, but the antithrombotic effects of CD36 deficiency were dependent on the dose of FeCl 3 used to induce injury (3) and platelet transfusion studies revealed that they were in part platelet dependent. Furthermore, CD36-mediated signaling through specific Src family kinases and MAPKs was shown to promote platelet activation after vascular injury (4). The endogenous CD36 ligands generated during FeCl 3 -induced injury include endothelial cellderived microparticles (EMPs), which we showed bind specifically to platelet CD36 and enhance platelet reactivity (3).

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Endothelin-1 decreases CD36 protein expression in vascular smooth muscle cells

Cited by 19 publications

References 44 publications

Intercellular adhesion molecule-4 and CD36 are implicated in the abnormal adhesiveness of sickle cell SAD mouse erythrocytes to endothelium

Intercellular adhesion molecule-4 and CD36 are implicated in the abnormal adhesiveness of sickle cell SAD mouse erythrocytes to endothelium

Circulating RNA Transcripts Identify Therapeutic Response in Cystic Fibrosis Lung Disease

CD36 participates in a signaling pathway that regulates ROS formation in murine VSMCs

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