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Your search keyword '"Azucena H. Kakazu"' showing total 2 results
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2 results on '"Azucena H. Kakazu"'

1. ELV-N32 and RvD6 isomer decrease pro-inflammatory cytokines, senescence programming, ACE2 and SARS-CoV-2-spike protein RBD binding in injured cornea

Author

Thang L. Pham, Jiucheng He, Azucena H. Kakazu, Jorgelina Calandria, Khanh V. Do, Robert Nshimiyimana, Ting F. Lam, Nicos A. Petasis, Haydee E. P. Bazan, and Nicolas G. Bazan

Subjects
Medicine, Science
Abstract

Abstract The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection that causes coronavirus disease 2019 (COVID-19) has resulted in a pandemic affecting the most vulnerable in society, triggering a public health crisis and economic collapse around the world. Effective treatments to mitigate this viral infection are needed. Since the eye is a route of virus entrance, we use an in vivo rat model of corneal inflammation as well as human corneal epithelial cells (HCEC) in culture challenged with IFNγ as models of the eye surface to study this issue. We explore ways to block the receptor-binding domain (RBD) of SARS-CoV-2 Spike (S) protein to angiotensin-converting enzyme 2 (ACE2). We found that the lipid mediators, elovanoid (ELV)-N32 or Resolvin D6-isomer (RvD6i) decreased the expression of the ACE2 receptor, furin, and integrins in damaged corneas or IFNγ-stimulated HCEC. There was also a concomitant decrease in the binding of Spike RBD with the lipid treatments. Using RNA-seq analysis, we uncovered that the lipid mediators also attenuated the expression of pro-inflammatoy cytokines participating in hyper-inflammation and senescence programming. Thus, the bioactivity of these lipid mediators will contribute to open therapeutic avenues to counteract virus attachment and entrance to the body.

Published
2021
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2. ELV-N32 and RvD6 isomer decrease pro-inflammatory cytokines, senescence programming, ACE2 and SARS-CoV-2-spike protein RBD binding in injured cornea

Author

Jiucheng He, Jorgelina M. Calandria, Azucena H Kakazu, Robert Nshimiyimana, Ting F. Lam, Haydee E. P. Bazan, Nicos A. Petasis, Nicolas G. Bazan, Khanh Do, and Thang Luong Pham

Subjects
Senescence, Male, Docosahexaenoic Acids, Science, Virus Attachment, Corneal inflammation, Virus, Article, Proinflammatory cytokine, Rats, Sprague-Dawley, chemistry.chemical_compound, Protein Domains, Drug Discovery, Medicine, Animals, Humans, Receptor, Furin, Cells, Cultured, Cellular Senescence, Multidisciplinary, biology, business.industry, SARS-CoV-2, Epithelium, Corneal, COVID-19, Epithelial Cells, Lipid signaling, Virus Internalization, Rats, Lipoxins, Disease Models, Animal, chemistry, Immunology, Spike Glycoprotein, Coronavirus, biology.protein, Cytokines, Angiotensin-Converting Enzyme 2, business, Resolvin, Corneal Injuries, Protein Binding, Signal Transduction
Abstract

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection that causes coronavirus disease 2019 (COVID-19) has resulted in a pandemic affecting the most vulnerable in society, triggering a public health crisis and economic collapse around the world. Effective treatments to mitigate this viral infection are needed. Since the eye is a route of virus entrance, we use an in vivo rat model of corneal inflammation as well as human corneal epithelial cells (HCEC) in culture challenged with IFNγ as models of the eye surface to study this issue. We explore ways to block the receptor-binding domain (RBD) of SARS-CoV-2 Spike (S) protein to angiotensin-converting enzyme 2 (ACE2). We found that the lipid mediators, elovanoid (ELV)-N32 or Resolvin D6-isomer (RvD6i) decreased the expression of the ACE2 receptor, furin, and integrins in damaged corneas or IFNγ-stimulated HCEC. There was also a concomitant decrease in the binding of Spike RBD with the lipid treatments. Using RNA-seq analysis, we uncovered that the lipid mediators also attenuated the expression of pro-inflammatoy cytokines participating in hyper-inflammation and senescence programming. Thus, the bioactivity of these lipid mediators will contribute to open therapeutic avenues to counteract virus attachment and entrance to the body.

Published
2021

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