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Research
Phoenixin 20 Prevents ox-LDL-Induced Attachment of Monocytes to Human Aortic Endothelial cells (HAECs): A Protective Implication in Atherosclerosis
Lichao Ye
Second Attached Hospital of Fujian Medical University
Corresponding Author
ORCiD: https://orcid.org/0000-0001-7706-5644
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: The cause of atherosclerosis is not known, and therefore the current treatment options are limited. In the present study, we aimed to investigate the effects of Phoenixin 20 and its receptor G protein-coupled receptor 173 (GPR173) against ox-LDL- induced endothelial dysfunction.
Materials and Methods: Human aortic endothelial cells (HAECs) were treated with 10 μg/ml ox-LDL in the presence or absence of phoenixin 20. Gene expression of GPR173, ICAM-1, VCAM-1, IL-1β, IL-8, MCP-1, and NOX-4 were measured by real time PCR. Protein expression was assayed by western blot analysis. Secretions of pro-inflammatory cytokines were measured by ELISA. The attachment of THP-1 monocytes to HAECs was detected using calcein-AM staining. Transcriptional activity of NF-κB was measured using dual-luciferase reporter assay.
Results: Our findings indicate that ox-LDL significantly lowered the expression of GPR173 in HAECs and triggered an increase in ROS, NOX-4, and proinflammatory cytokine expression. Importantly, we demonstrate that agonism of GPR173 using phoenixin 20 significantly ameliorated these harmful effects of ox-LDL. We also show that agonism of GPR173 can prevent the attachment of monocytes to endothelial cells, which is an important therapeutic approach to prevent atherogenesis.
Conclusion: Here, for the first time to our knowledge, we provide a basis for future research on the role of GPR173 as a new potential treatment against atherosclerosis.
Keywords
Atherosclerosis, oxidized low-density lipoprotein (ox-LDL), GPR173, Phoenixin 20, endothelial cells
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Research
Phoenixin 20 Prevents ox-LDL-Induced Attachment of Monocytes to Human Aortic Endothelial cells (HAECs): A Protective Implication in Atherosclerosis
Lichao Ye
Second Attached Hospital of Fujian Medical University
Corresponding Author
ORCiD: https://orcid.org/0000-0001-7706-5644
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 18 Sep, 2020
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cell & Tissue Engineering
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: The cause of atherosclerosis is not known, and therefore the current treatment options are limited. In the present study, we aimed to investigate the effects of Phoenixin 20 and its receptor G protein-coupled receptor 173 (GPR173) against ox-LDL- induced endothelial dysfunction.
Materials and Methods: Human aortic endothelial cells (HAECs) were treated with 10 μg/ml ox-LDL in the presence or absence of phoenixin 20. Gene expression of GPR173, ICAM-1, VCAM-1, IL-1β, IL-8, MCP-1, and NOX-4 were measured by real time PCR. Protein expression was assayed by western blot analysis. Secretions of pro-inflammatory cytokines were measured by ELISA. The attachment of THP-1 monocytes to HAECs was detected using calcein-AM staining. Transcriptional activity of NF-κB was measured using dual-luciferase reporter assay.
Results: Our findings indicate that ox-LDL significantly lowered the expression of GPR173 in HAECs and triggered an increase in ROS, NOX-4, and proinflammatory cytokine expression. Importantly, we demonstrate that agonism of GPR173 using phoenixin 20 significantly ameliorated these harmful effects of ox-LDL. We also show that agonism of GPR173 can prevent the attachment of monocytes to endothelial cells, which is an important therapeutic approach to prevent atherogenesis.
Conclusion: Here, for the first time to our knowledge, we provide a basis for future research on the role of GPR173 as a new potential treatment against atherosclerosis.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
Figure 8