Alpha-1 antitrypsin inhibits fractalkine-mediated monocyte-lung endothelial cell interactions-Reference-Cited by-同舟云学术

Alpha-1 antitrypsin inhibits fractalkine-mediated monocyte-lung endothelial cell interactions

Published:2023-12-01 Issue:6 Volume:325 Page:L711-L725
ISSN:1040-0605
Container-title:American Journal of Physiology-Lung Cellular and Molecular Physiology
language:en
Short-container-title:American Journal of Physiology-Lung Cellular and Molecular Physiology

Author:

Mikosz Andrew¹,Ni Kevin¹²^ORCID,Gally Fabienne³^ORCID,Pratte Katherine A.¹^ORCID,Winfree Seth⁴⁵^ORCID,Lin Qiong⁶,Echelman Isabelle¹,Wetmore Brianna¹,Cao Danting¹⁷,Justice Matthew J.¹,Sandhaus Robert A.¹,Maier Lisa¹⁷,Strange Charlie⁸,Bowler Russell P.¹⁷,Petrache Irina¹⁴⁷^ORCID,Serban Karina A.¹⁴⁷^ORCID

Affiliation:

1. Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, National Jewish Health, Denver, Colorado, United States

2. Medical Scientist Training Program, Indiana University School of Medicine, Indianapolis, Indiana, United States

3. Department of Immunology and Genomic Medicine, National Jewish Health, Denver, Colorado, United States

4. Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, Indiana University, Indianapolis, Indiana, United States

5. Department of Anatomy, Cell Biology and Physiology, Indiana University, Indianapolis, Indiana, United States

6. Department of Medicine, Fuzhou First Hospital Affiliated with Fujian Medical University, Fuzhou, Fujian, China

7. Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, University of Colorado, Anschutz Medical Center, Aurora, Colorado, United States

8. Department of Medicine, Division of Pulmonary, Critical Care, Allergy and Sleep Medicine, Medical University of South Carolina, Charleston, South Carolina, United States

Abstract

Our novel findings that AAT and other inhibitors of TACE, the sheddase that controls full-length fractalkine (CX3CL1) endothelial expression, may provide fine-tuning of the CX3CL1-CX3CR1 axis specifically involved in endothelial-monocyte cross talk and leukocyte recruitment to the alveolar space, suggests that AAT and inhibitors of sCX3CL1 signaling may be harnessed to reduce lung inflammation.

Funder

CU | UC Denver | Colorado Clinical and Translational Sciences Institute

Flight Attendant Medical Research Institute

HHS | NIH | NIAID | Division of Microbiology and Infectious Diseases, National Institute of Allergy and Infectious Diseases

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

Alpha-1 Foundation

Publisher

American Physiological Society

Subject

Cell Biology,Physiology (medical),Pulmonary and Respiratory Medicine,Physiology

Link

https://journals.physiology.org/doi/pdf/10.1152/ajplung.00023.2023

Reference61 articles.

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1. Feeling good: welcoming the new editorial team for American Journal of Physiology-Lung Cellular and Molecular Physiology;American Journal of Physiology-Lung Cellular and Molecular Physiology;2024-01-01