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Functional characterization of human IL-8 in vascular stenosis using a novel humanized transgenic mouse model

*Corresponding author for this work
Scholary Output:
Contribution to journal
Article
Peer-review

Open access

Sustainable Development Goals

  • SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well

Abstract

IL-8 (aka interleukin 8, CXCL8) is a prototypic cytokine that is highly expressed in the diseased vessel wall and its plasma concentration is strongly associated with cardiovascular events. However, whether IL-8 plays a causative role in cardiovascular diseases remains largely unknown. In this study we used a human IL-8 transgenic (Tg) mouse strain with a bacterial artificial chromosome (BAC) integrated into its genome. This BAC encompasses 166 kb of sequence encompassing the human IL-8 gene locus as well as upstream and downstream DNA sequences containing regulatory elements. This BAC ensured a pathophysiologically regulated, rather than forced constitutive, expression of human IL-8 in the mouse. Tg mice were subjected to complete carotid ligation injury. IL-8 was highly expressed in the ligation-injured carotid artery from 3 days until 2 weeks after injury. As a result, exacerbated neointimal hyperplasia and increased Mac2 and PCNA positive cells were observed in Tg mice. To further confirm its role in promoting neointimal formation, IL-8 was neutralized by anti-IL8 treatment at the ligation site. Consequently, the size of neointima was significantly reduced. Our results provided new insights into the regulation and function of IL-8 in response to vascular insult and during neointima formation.

Publication Information

Output type

Scholary Output:
Contribution to journal
Article
Peer-review

Original language

English (US)

Article number

107438

Journal (Volume, Issue Number)

Vascular Pharmacology (Volume 157)

Publication milestones

  • Published - 12/2024

Publication status

Published - 12/2024

ISSN

1537-1891

Publication IDs

  • Scopus: 85208035013
  • PubMed: 39486776

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Scopus
citations
Fractional count
2
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0.33
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4
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0.67
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2
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1

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5
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Funding Details

This work was supported by American Heart Association ( TPA1141836 , SCEFIA1156682 and CDA34110319 to Wei Zhang; EIA961515 to Xiaochun Long; and CDA938570 to Kunzhe Dong), Augusta University Intramural Grants Program (IGPP00051 to Wei Zhang), and National Institutes of Health ( R01HL122686 and R01HL139794 to Xiaochun Long).
FundersFunding numbersAugusta University
IGPP00051
NIH
R01HL139794, R01HL122686
AHA
TPA1141836, EIA961515, SCEFIA1156682, CDA938570, CDA34110319