<scp>CCL</scp>23 is a promising biomarker of injury in patients with ischaemic stroke

Bonaventura, Aldo; Montecucco, Fabrizio

doi:10.1111/joim.12742

Cited by 11 publications

(8 citation statements)

References 10 publications

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“…The nine biomarkers identified in the present study were previously reported in ischemic stroke which involved the process of inhibiting development of atherosclerotic plaques, vascular remodeling, neural regeneration, and inflammatory response [ 16 – 25 ]. For example, IGFBP-6 and IL-5 were reported to be associated with inhibiting development of atherosclerotic plaques [ 26 – 29 ], LYVE-1 and PDGF-AA were beneficial to vascular remodeling and neural regeneration, respectively [ 16 – 18 ], while CCL-23, CXCL-12, ST-2, and TNF-α were reported to promote and worsen the inflammatory response: CCL-23, CXCL-12, and TNF-α played pro-inflammatory role [ 19 – 21 ], while ST-2 prevented anti-inflammatory effect of IL-33 [ 22 , 23 ]. In addition, PAI has an effect on inhibiting fibrinolysis in patients treated with tissue plasminogen activator [ 24 , 25 ].…”

Section: Discussionmentioning

confidence: 99%

“…Based on functional enrichment analysis, mononuclear cell migration, receptor ligand activity, platelet alpha granule lumen, and cytokine-cytokine receptor interaction were significantly enriched items. After brain injury, CCL-23 and CXCL-12 modulate immune response through promoting migration of monocytes to the local sites of injury [ 19 , 20 ]. As the result of monocytes migration, inflammatory cytokines released from microglia, such as TNF-α, modulate infarct evaluation [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

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Association of serum biomarkers with early neurologic improvement after intravenous thrombolysis in ischemic stroke

et al. 2022

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Background Early neurologic improvement (ENI) after intravenous thrombolysis is associated with favorable outcome, but associated serum biomarkers were not fully determined. We aimed to investigate the issue based on a prospective cohort. Methods In INTRECIS study, five centers were designed to consecutively collect blood sample from enrolled patients. The patients with ENI and without ENI were matched by propensity score matching with a ratio of 1:1. Preset 49 biomarkers were measured through microarray analysis. Enrichment of gene ontology and pathway, and protein-protein interaction network were analyzed in the identified biomarkers. Results Of 358 patients, 19 patients with ENI were assigned to ENI group, while 19 matched patients without ENI were assigned to Non ENI group. A total of nine biomarkers were found different between two groups, in which serum levels of chemokine (C-C motif) ligand (CCL)-23, chemokine (C-X-C motif) ligand (CXCL)-12, insulin-like growth factor binding protein (IGFBP)-6, interleukin (IL)-5, lymphatic vessel endothelial hyaluronan receptor (LYVE)-1, plasminogen activator inhibitor (PAI)-1, platelet-derived growth factor (PDGF)-AA, suppression of tumorigenicity (ST)-2, and tumor necrosis factor (TNF)-α were higher in the ENI group, compared with those in the Non ENI group. Conclusions We found that serum levels of CCL-23, CXCL-12, IGFBP-6, IL-5, LYVE-1, PAI-1, PDGF-AA, ST-2, and TNF-α at admission were associated with post-thrombolytic ENI in stroke. The role of biomarkers warrants further investigation. Trial registration Clinical Trial Registration: https://www.clinicaltrials.gov; identifier: NCT02854592.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Association of serum biomarkers with early neurologic improvement after intravenous thrombolysis in ischemic stroke

et al. 2022

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“…CCL23 has been reported to be associated with brain injury, immune response, systemic sclerosis, rhinosinusitis and other diseases [ 11 , 36 , 37 ]. However, to the best of our knowledge, the study of CCL23 and HCC has been limited to network data analysis.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effect of CC chemokine ligand 23 (CCL23)/ transcription factor activating enhancer binding protein 4 (TFAP4) on cell proliferation, invasion and angiogenesis in hepatocellular carcinoma

Wang

Dai

et al. 2022

Bioengineered

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Hepatocellular carcinoma (HCC) is a highly vascularized solid tumor with a fast growth rate. According to bioinformatics analysis, CC chemokine ligand 23 (CCL23) has clinical significance for survival and prognosis in HCC. The online databases TCGA and CCLE were used to analyze the expression level of CCL23, and its expression was also measured in HCC cell lines by RT-qPCR and Western blotting. The STRING database and co-immunoprecipitation were employed to evaluate the association between CCL23 and transcription factor activating enhancer binding protein 4 (TFAP4). Overexpression plasmids for CCL23 (Ov-CCL23) and TFAP4 (Ov-TFAP4) were transfected into Huh-7 cells to detect TFAP4 expression. Huh-7 cells injected with OV-negative control (NC)/Ov-CCL23 or OV-NC/Ov-CCL23 plus Ov-TFAP4 were utilized to study the function of CCL23/TFAP4. Cell proliferation, invasion and human umbilical vein endothelial cell tube formation assays were conducted. The database revealed decreased expression of CCL23 in HCC and that it was commonly downregulated in HCC cell lines. TFAP4 expression was negatively correlated with CCL23. The overexpression of CCL23 inhibited the proliferation and invasion of Huh-7 cells, whereas TFAP4 blocked these effects. Similarly, the supernatant of CCL23-upregulated cells exhibited significantly lower tube formation potential, and low vascular endothelial growth factor A (VEGFA), VEGFRs expression compared with those of non-transfected Huh-7 cells, while TFAP4 plasmid co-transfected markedly increased these. Taken together, the present study suggests that CCL23 is expressed at low levels in HCC; it inhibits HCC cell proliferation, invasion and angiogenesis in vitro ; and its action is negatively associated with and can be blocked by TFAP4.

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“…and PDGF-AA were bene cial to vascular remodeling and neural regeneration, respectively, [20][21][22] while CCL-23, CXCL-12, ST-2, and TNF-α were reported to promote and worsen the in ammatory response: CCL-23, CXCL-12, and TNF-α played pro-in ammatory role; [23][24][25] and ST-2 prevented anti-in ammatory effect of IL-33. [26][27] In addition, PAI has an effect on inhibiting brinolysis in patients treated with tissue plasminogen activator.…”

Section: Discussionmentioning

confidence: 99%

“…Contributing to the in ammation after brain injury, CCL-23 and CXCL-12 modulate immune response through promoting migration of monocytes to the local sites of injury. [23][24] As the result of monocytes migration, releasing in ammatory cytokines from microglia, such as TNF-α, modulate infarct evaluation. 25 It is worthy to note that these cytokines seemed contradictory with ENI given their proin ammatory effects.…”

Section: Discussionmentioning

confidence: 99%

Association of Serum Biomarkers with Post-Thrombolytic Early Neurological Improvement in Stroke: A Comprehensive Protein Microarray Analysis From INTRECIS Study

Cui

Wang

Zhao

et al. 2022

Preprint

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Objective Early neurological improvement (ENI) after intravenous thrombolysis is associated with favorable outcome, but associated serum biomarkers were not fully determined. We aimed to investigate the issue in a prospective cohort. Methods In INTRECIS study, five centers were designed to consecutively collect the blood sample from enrolled patients. Enrolled patients with ENI and without ENI were matched by propensity score matching with the ratio of 1:1. Preset 49 biomarkers were measured by protein microarray analysis. Enrichment of Gene Ontology and pathway, and protein-protein interaction network were analyzed in the identified biomarkers. Results Of 358 patients, 19 occurred ENI, who were assigned as ENI group, while 19 matched patients without ENI were assigned as Non ENI group. A total of 9 biomarkers were found different, among which levels of chemokine (C-C motif) ligand (CCL)-23, chemokine (C-X-C motif) ligand (CXCL)-12, insulin-like growth factor binding protein (IGFBP)-6, interleukin (IL)-5, lymphatic vessel endothelial hyaluronan receptor (LYVE)-1, plasminogen activator inhibitor (PAI)-1, platelet-derived growth factor (PDGF)-AA, suppression of tumorigenicity (ST)-2, and tumor necrosis factor (TNF)-α were higher in ENI group, compared with those in Non ENI group. Interpretation: Our finding indicated that pretreatment serum CCL-23, CXCL-12, IGFBP-6, IL-5, LYVE-1, PAI-1, PDGF-AA, ST-2, and TNF-α levels were associated with post-thrombolytic ENI in ischemic stroke. The role of these biomarkers warrant further investigation. Registration-URL : https://www.clinicaltrials.gov; Unique identifier: NCT02854592.

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CCL23 is a promising biomarker of injury in patients with ischaemic stroke

Abstract: http://onlinelibrary.wiley.com/doi/10.1111/joim.12738/full.

Cited by 11 publications

References 10 publications

Association of serum biomarkers with early neurologic improvement after intravenous thrombolysis in ischemic stroke

Association of serum biomarkers with early neurologic improvement after intravenous thrombolysis in ischemic stroke

Inhibitory effect of CC chemokine ligand 23 (CCL23)/ transcription factor activating enhancer binding protein 4 (TFAP4) on cell proliferation, invasion and angiogenesis in hepatocellular carcinoma

Association of Serum Biomarkers with Post-Thrombolytic Early Neurological Improvement in Stroke: A Comprehensive Protein Microarray Analysis From INTRECIS Study

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