한빛사 논문
J. Park1, M.-Y. Park1, Y. Kim1, Y. Jun2, U. Lee3 and C.-M. Oh1
From the 1Department of Biomedical Science and Engineering, Gwangju Institute of Science and Technology,Gwangju, Korea, 2Cell Logistics Research Center, Gwangju Institute of Science and Technology, Gwangju, Korea and 3Department of Cardiac Surgery, Boston Children’s Hospital, Boston, MA, USA
Address correspondence to C.-M. Oh
Abstract
Background: Apelin is an endogenous neuropeptide that binds to the G-protein-coupled receptor (APJ) and participates in a variety of physiological processes in the heart, lungs, and other peripheral organs. Intriguingly, [Pyr1]-Apelin-13, a highly potent pyroglutamic form of apelin, has the potential to bind to and be degraded by angiotensin-converting enzyme 2 (ACE2). ACE2 is known to operate as a viral receptor in the early stages of severe acute respiratory coronavirus (SARS-CoV-2) infection.
Aim: This study aimed to determine if apelin protects against SARS-CoV-2 infection by inhibiting ACE2 binding to SARS-CoV-2 spike protein.
Design and methods: To determine whether [Pyr1]-Apelin-13 inhibits ACE2 binding to the SARS-CoV-2 spike protein (S protein), we performed a cell-to-cell fusion assay using ACE2-expressing cells and S protein-expressing cells and a pseudovirus-based inhibition assay. We then analyzed publicly available transcriptome data while focusing on the beneficial effects of apelin on the lungs.
Results: We found that [Pyr1]-Apelin-13 inhibits cell-to-cell fusion mediated by ACE2 binding to the S protein. In this experiment, [Pyr1]-Apelin-13 protected human bronchial epithelial cells, infected with pseudo-typed lentivirus producing S protein, against viral infection. In the presence of [Pyr1]-Apelin-13, the level of viral spike protein expression was also reduced in a concentration-dependent manner. Transcriptome analysis revealed that apelin may control inflammatory responses to viral infection by inhibiting the nuclear factor kappa B pathway.
Conclusion: Apelin is a potential therapeutic candidate against SARS-CoV-2 infection.
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