Recent Advancements in CD47 Signal Transduction Pathways Involved in Vascular Diseases

Dou, Manman; Chen, Ying; Hu, Jian; Ma, Di; Xing, Yingqi

doi:10.1155/2020/4749135

Cited by 11 publications

(7 citation statements)

References 76 publications

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“…CD47 acts as a "do not eat me" receptor by interacting with SIRPα on the healthy macrophage surface membrane and prevents phagocytosis by triggering a dephosphorylation cascade [7][8][9]. Vascular growth factor (VEGF) and its receptor (VEGFR2) can be activated by TSP-1 and CD47 in combination to stimulate angiogenesis, and the interaction between CD47 and integrin αVβ3 enhances neovascularization to allow tumor growth [10]. Studies have shown that the overall survival (OS) and progression-free survival (PFS) of DLBCL patients, especially those with the activated B-cell-like (ABC) subtype, are significantly reduced when both CD47 on tumor cells and SIRPα in stromal cells are upregulated or when only SIRPα expression is increased.…”

Section: Applications Of Cd47 In Clinical Therapiesmentioning

confidence: 99%

Therapy Strategy of CD47 in Diffuse Large B-Cell Lymphoma (DLBCL)

Zhang

Fan

et al. 2021

Disease Markers

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At present, the use of the common chemotherapy regimen CHOP/R-CHOP for diffuse large B-cell lymphoma (DLBCL) has some shortcomings, especially for relapsed and refractory DLBCL. CD47 is now considered as a prominent target in cancer therapies, and CD47 blockade mainly inhibits the CD47-SIRPα axis to prevent tumor immune escape. Here, we evaluated the effects of the latest CD47 antibodies reported and the correlations of closely related genes with CD47 in this disease. In the future, therapeutic strategies for DLBCL will focus on multitarget antibody combined treatment and multigene joint attacks.

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Section: Applications Of Cd47 In Clinical Therapiesmentioning

confidence: 99%

Therapy Strategy of CD47 in Diffuse Large B-Cell Lymphoma (DLBCL)

Zhang

Fan

et al. 2021

Disease Markers

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“…CD47 is a “don't eat me signal” on the cell surface and is involved in a range of cellular processes, including apoptosis , proliferation , adhesion , and migration . 26 EndoV is shown to cleave RNA at inosines, and the high expression of CD47 in the EndoV −/− mice could be attributed to a lack of transcript degradation in the absence of ENDOV. However, inspection of adenosine‐to‐inosine editing (observed as Adenosine to Guanine mutations) in the RNA sequencing data when compared with the mouse genomic sequence (GRCm38.p6, Ensembl release 98) 18 in the CD47 transcript showed no adenosine‐to‐inosine editing in either wild‐type or EndoV −/− mRNA (data not shown).…”

Section: Resultsmentioning

confidence: 99%

Endonuclease V Regulates Atherosclerosis Through C‐C Motif Chemokine Ligand 2‐Mediated Monocyte Infiltration

Kong

Huse

Yang

et al. 2021

JAHA

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Background In cardiovascular diseases, atherosclerotic disorder are the most frequent and important with respect to morbidity and mortality. Inflammation mediated by immune cells is central in all parts of the atherosclerotic progress, and further understanding of the underlying mechanisms is needed. Growing evidence suggests that deamination of adenosine‐to‐inosine in RNA is crucial for a correct immune response; nevertheless, the role of adenosine‐to‐inosine RNA editing in atherogenesis has barely been studied. Several proteins have affinity for inosines in RNA, one being ENDOV (endonuclease V), which binds and cleaves RNA at inosines. Data on ENDOV in atherosclerosis are lacking. Methods and Results Quantitative polymerase chain reaction on ENDOV mRNA showed an increased level in human carotid atherosclerotic plaques compared with control veins. Inosine‐ribonuclease activity as measured by an enzyme activity assay is detected in immune cells relevant for the atherosclerotic process. Abolishing EndoV in atherogenic apolipoprotein E‐deficient ( ApoE −/− ) mice reduces the atherosclerotic plaque burden, both in size and lipid content. In addition, in a brain stroke model, mice without ENDOV suffer less damage than control mice. Finally, lack of EndoV reduces the recruitment of monocytes to atherosclerotic lesions in atherogenic ApoE −/− mice. Conclusions ENDOV is upregulated in human atherosclerotic lesions, and data from mice suggest that ENDOV promotes atherogenesis by enhancing the monocyte recruitment into the atherosclerotic lesion, potentially by increasing the effect of CCL2 activation on these cells.

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“… 116 , 117 Plaque cells highly express an antiphagocytosis ligand, Cluster of Differentiation 47 (CD47), on their surfaces, which inhibits them from being cleared by efferocytosis. 118 In fact, mice treated with anti-CD47 antibodies restored efferocytosis and prevented atherosclerosis. 119 However, these mice also developed anemia due to the antibody’s effects of off-target clearance of red blood cells in the spleen.…”

Section: Emerging Anti-atherosclerotic Therapiesmentioning

confidence: 99%