Cited by 124Chemokine receptors and signalingRenin-Angiotensin System StudiesCoagulation, Bradykinin, Polyphosphates, and Angioedema

Angiotensin II Induces Neutrophil Accumulation In Vivo Through Generation and Release of CXC Chemokines

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Nabah, Yafa Naim Abu, Mateo, Teresa, Estellés, Rossana, Mata, Manuel, Zagorski, John, Sarau, Henry, Cortijo, Julio, Morcillo, Esteban J. +2 more·2004·Circulation

Abstract

Background Angiotensin II (Ang II) is implicated in the development of cardiac ischemic disorders in which prominent neutrophil accumulation occurs. Ang II can be generated intravascularly by the renin-angiotensin system or extravascularly by mast cell chymase. In this study, we characterized the ability of Ang II to induce neutrophil accumulation. Methods and results Intraperitoneal administration of Ang II (1 nmol/L) induced significant neutrophil recruitment within 4 hours (13.3+/-2.3x10(6) neutrophils per rat versus 0.7+/-0.5x10(6) in control animals), which disappeared by 24 hours. Maximal levels of CXC chemokines were detected 1 hour after Ang II injection (577+/-224 pmol/L cytokine-inducible neutrophil chemoattractant [CINC]/keratinocyte-derived chemokine [KC] versus 5+/-3, and 281+/-120 pmol/L macrophage inflammatory protein [MIP-2] versus 14+/-6). Intravital microscopy within the rat mesenteric microcirculation showed that the short-term (30 to 60 minutes) leukocyte-endothelial cell interactions induced by Ang II were attenuated by an anti-rat CINC/KC antibody and nearly abolished by the CXCR2 antagonist SB-517785-M. In human umbilical vein endothelial cells (HUVECs) or human pulmonary artery media in culture, Ang II induced interleukin (IL)-8 mRNA expression at 1, 4, and 24 hours and the release of IL-8 at 4 hours through interaction with Ang II type 1 receptors. When HUVECs were pretreated with IL-1 for 24 hours to promote IL-8 storage in Weibel-Palade bodies, the…

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Crossref · 10.1161/01.cir.0000148824.93600.f3

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  • ATR1 also increases reactive oxygen species from mitochondria in monocytes/macrophages leading to DNA damage and apoptosis of T cells resulting in endothelial injury and lymphopenia.

    “ATR1 also increases reactive oxygen species from mitochondria in monocytes/macrophages leading to DNA damage and apoptosis of T cells resulting in endothelial injury and lymphopenia.”

    From COVID-19, Myocarditis and Pericarditis (2023) · cites this paper as [59]

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Authors
Nabah, Y. N. A., Mateo, T., Estellés, R., Mata, M., Zagorski, J., Sarau, H., Cortijo, J., Morcillo, E. J., Jose, P. J., & Sanz, M.-J.
Affiliations
  • Universitat de València (ES)
  • From the Department of Pharmacology (Y.N.A.N., T.M., R.E., M.M., J.C., E.J.M., M.-J.S.), Faculty of Medicine, University of Valencia, Valencia, Spain; the Carolinas Medical Center (J.Z.), Charlotte, NC; GlaxoSmithKline (H.S.), King of Prussia, Pa; the Valencia General Hospital Foundation, General Hospital of Valencia (J.C.), Valencia, Spain; and the Department of Leukocyte Biology (P.J.J.), School of Biomedical Sciences, Imperial College, London, UK.
Venue
Circulation
Published
2004-12-07
Volume
110
Issue
23
Pages
3581-3586
ISSN
  • 0009-7322 (ISSN-L)
  • 1524-4539
OpenAlex
W2136025343
Cited by
124
References
25
Citations by year
2026: 1 · 2025: 3 · 2024: 6 · 2023: 4 · 2022: 10 · 2021: 8 · 2020: 8 · 2019: 4 · 2018: 2 · 2017: 2 · 2016: 6 · 2015: 9 · 2014: 6 · 2013: 5 · 2012: 1
FWCI
2.73
Type
journal article
Language
en
Open access
Licence
cc-by-nc
Locations
  • Circulation (publishedVersion)
  • PubMed (publishedVersion)
  • Repository of Digital Objects for Teaching Research and Culture (University of Valencia) (submittedVersion, cc-by-nc)
Funders
  • Ministerio de Educación, Cultura y Deporte (SAF 2002-01482)
  • Generalitat Valenciana
  • Ministerio de Ciencia y Tecnología
Topics
  • Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
  • Health Sciences › Medicine › Genetics › Coagulation, Bradykinin, Polyphosphates, and Angioedema
Keywords
angiotensin II, neutrophil accumulation, CXC chemokines, CXCL2, interleukin-8, CXCR2, leukocyte-endothelium interaction, chymase, renin-angiotensin system, acute myocardial infarction, neutrophil infiltration, interleukin-1, Weibel-Palade bodies, endothelial cells
MeSH terms
Angiotensin II, Animals, Cell Adhesion, Cells, Cultured, Humans, Leukocytes, Male, Mesentery, Microcirculation, Peritoneal Cavity, Pulmonary Artery, RNA, Messenger, Umbilical Cord, Interleukin-8, Rats, Sprague-Dawley, Chemokines, CXC, Neutrophil Infiltration, Endothelial Cells, Rats

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