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CD93 in macrophages: A novel target for atherosclerotic plaque imaging?

ABSTRACT: Noninvasive imaging atherosclerotic (AS) plaque is of great importance for early diagnosis. Recently, CD93 in MΦ was linked to atherosclerosis development. Herein, we have investigated whether CD93 in MΦ is a potential novel target for atherosclerotic plaque imaging. CD93^hi and CD93^lo MΦ were prepared with or without LPS stimulation, before biological activity was evaluated. A rat AS model was produced with left carotid artery clamped. Whole-body/ex vivo phosphor autoradiography of the artery and biodistribution were investigated after incorporation of ³ H-2-DG into CD93^hi and CD93^lo MΦ or after ¹²⁵ I-α-CD93 (¹²⁵ I-anti-CD93mAb) injection. The plaque tissue was subjected to CD93/CD68 immunofluorescence/immunohistochemistry staining. CD93^hi and CD93^lo MΦ cells were successfully prepared without significant effect on bioactivity after incorporative labelled with ³ H-2-DG. The AS model was successfully established. Biodistribution studies showed that adoptive transfer of ³ H-2-DG-CD93^hi MΦ or ¹²⁵ I- α-CD93 injection resulted in accumulation of radioactivity within the atherosclerotic plaque in the clamped left carotid artery. T/NT (target/non-target, left/right carotid artery) ratio was higher in the ³ H-2-DG-CD93^hi MΦ adoptive transfer group than in the ³ H-2-DG-CD93^lo MΦ group (p < .05). Plaque radioactivity in the ¹²⁵ I-α-CD93 injection group was significantly higher than in the ¹²⁵ I-IgG control group (p < .01). The higher radioactivity accumulated in the clamped left carotid artery was confirmed by phosphor autoradiography. More importantly, CD93/CD68 double-positive MΦ accumulated at the atherosclerotic plaque in ³ H-2-DG-CD93^hi MΦ adoptive transfer group, which correlated with plaque radioactivity (r = .99, p < .01). In summary, both adoptive-transferred ³ H-2-DG-labelled CD93^hi MΦ and ¹²⁵ I-α-CD93 injection specifically targeted CD93 in atherosclerotic plaque. CD93 is a potential target in atherosclerotic plaque imaging.

SUBMITTER: Su C

PROVIDER: S-EPMC8995462 | biostudies-literature | 2022 Apr

REPOSITORIES: biostudies-literature

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CD93 in macrophages: A novel target for atherosclerotic plaque imaging?

Su Chen C Han Yeming Y Qu Bin B Zhang Chao C Liang Ting T Gao Feng F Hou Guihua G

Journal of cellular and molecular medicine 20220215 8

Noninvasive imaging atherosclerotic (AS) plaque is of great importance for early diagnosis. Recently, CD93 in MΦ was linked to atherosclerosis development. Herein, we have investigated whether CD93 in MΦ is a potential novel target for atherosclerotic plaque imaging. CD93<sup>hi</sup> and CD93<sup>lo</sup> MΦ were prepared with or without LPS stimulation, before biological activity was evaluated. A rat AS model was produced with left carotid artery clamped. Whole-body/ex vivo phosphor autoradiog ...[more]

PMID: 35166040

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Project description:BACKGROUND:Atherosclerotic plaque rupture is the culprit event which underpins most acute vascular syndromes such as acute myocardial infarction. Novel biomarkers of plaque rupture could improve biological understanding and clinical management of patients presenting with possible acute vascular syndromes but such biomarker(s) remain elusive. Investigation of biomarkers in the context of de novo plaque rupture in humans is confounded by the inability to attribute the plaque rupture as the source of biomarker release, as plaque ruptures are typically associated with prompt down-stream events of myocardial necrosis and systemic inflammation. METHODS:We developed a novel approach to identify potential biomarkers of plaque rupture by integrating plaque imaging, using optical coherence tomography, with both plaque and plasma proteomic analysis in a human model of angioplasty-induced plaque disruption. RESULTS:We compared two pairs of coronary plaque debris, captured by a FilterWire Device, and their corresponding control samples and found matrix metalloproteinase 9 (MMP9) to be significantly enriched in plaque. Plaque contents, as defined by optical coherence tomography, affect the systemic changes of MMP9. Disruption of lipid-rich plaque led to prompt elevation of plasma MMP9, whereas disruption of non-lipid-rich plaque resulted in delayed elevation of plasma MMP9. Systemic MMP9 elevation is independent of the associated myocardial necrosis and systemic inflammation (measured by Troponin I and C-reactive protein, respectively). This information guided the selection of a subset of subjects of for further label free proteomics analysis by liquid chromatography tandem mass spectrometry (LC-MS/MS). We discovered five novel, plaque-enriched proteins (lipopolysaccharide binding protein, Annexin A5, eukaryotic translocation initiation factor, syntaxin 11, cytochrome B5 reductase 3) to be significantly elevated in systemic circulation at 5 min after plaque disruption. CONCLUSION:This novel approach for biomarker discovery in human coronary artery plaque disruption can identify new biomarkers related to human coronary artery plaque composition and disruption.

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CD93 in macrophages: A novel target for atherosclerotic plaque imaging?

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CD93 in macrophages: A novel target for atherosclerotic plaque imaging?

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