Endothelial cells overexpressing CXCR1/2 are renoprotective in rats with acute kidney injury

Author:

Xing Dongqi1ORCID,Hage Fadi G.23,Feng Wenguang4,Guo Yuanyuan1,Oparil Suzanne2,Sanders Paul W.453ORCID

Affiliation:

1. Division of Pulmonary, Allergy and Critical Care Medicine, Lung Health Center, University of Alabama at Birmingham, Birmingham, Alabama, United States

2. Vascular Biology and Hypertension Program, Division of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, Alabama, United States

3. Birmingham Veterans Affairs Health Care System, Birmingham, Alabama, United States

4. Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, United States

5. Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, Alabama, United States

Abstract

Inflammation facilitates kidney ischemia-reperfusion (I/R) injury. Endothelial cells (ECs) that were modified to overexpress (C-X-C motif) chemokine receptor (CXCR)1/2 (CXCR1/2-ECs) were injected immediately following kidney I/R injury. The interaction of CXCR1/2-ECs, but not ECs transduced with an empty adenoviral vector, with injured kidney tissue preserved kidney function and reduced production of inflammatory markers, capillary rarefaction, and interstitial fibrosis. The study highlights a functional role for the C-X-C chemokine pathway in kidney damage following I/R injury.

Funder

HHS | NIH | National Heart, Lung, and Blood Institute

HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases

U.S. Department of Veterans Affairs

Publisher

American Physiological Society

Subject

Physiology

Cited by 2 articles. 订阅此论文施引文献 订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献

1. Immunological alterations in the endothelial barrier: a new predictive and therapeutic paradigm for sepsis;Expert Review of Clinical Immunology;2024-06-11

2. Guidelines on antibody use in physiology research;American Journal of Physiology-Renal Physiology;2024-03-01

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