ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012
CXCR4 regulates migration of lung alveolar epithelial cells through activation of Rac1 and matrix metalloproteinase-2.
Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
42 citing papers in PubMed, 62 citations in OpenAlex.
- From Heterogeneity to Plasticity: Endothelial Dynamics in Lung Disease.Pulmonary circulation · 2026Review
- Decoding Rho GTPase signalling networks in directed cell migration.Frontiers in cell and developmental biology · 2026Review
- Bioprinted Ventilated 3D Alveoliform Epithelial Sacculoids.Research square · 2025Article
- The CXCL12/CXCR4 Axis in Sepsis-Induced Acute Lung Injury: Mechanisms and Therapeutic Potential.Current issues in molecular biology · 2025Review
- G protein-coupled receptors as novel therapeutic targets in non-small-cell lung cancer.Medical review (2021) · 2025Review
- Article
- Article
- Single-Cell Characterization of Pulmonary Nodules Implicates Suppression of Immunosurveillance across Early Stages of Lung Adenocarcinoma.Cancer research · 2023Article
- Proteolytic inactivation of CXCL12 in the lungs and circulation of COVID-19 patients.Cellular and molecular life sciences : CMLS · 2023Article
- Pathophysiology of Sepsis and Genesis of Septic Shock: The Critical Role of Mesenchymal Stem Cells (MSCs).International journal of molecular sciences · 2022Review
- C-X-C-Chemokine-Receptor-Type-4 Inhibitor AMD3100 Attenuates Pulmonary Inflammation and Fibrosis in Silicotic Mice.Journal of inflammation research · 2022Article
- CXCR4 and CXCR7 Inhibition Ameliorates the Formation of Platelet-Neutrophil Complexes and Neutrophil Extracellular Traps through Adora2b Signaling.International journal of molecular sciences · 2021Article
- Review
- CXCR4 Knockdown Via CRISPR/CAS9 in a Tumor-Associated Macrophage Model Decreases Human Breast Cancer Cell Migration.Cureus · 2021Article
- Predictive and Prognostic Biomarkers for Lung Cancer Bone Metastasis and Their Therapeutic Value.Frontiers in oncology · 2021Review
- CXCR4Respiratory research · 2020Article
- High COAmerican journal of respiratory cell and molecular biology · 2020Article
- Hypercapnia Regulates Gene Expression and Tissue Function.Frontiers in physiology · 2020Review
- Inhibition of CXCR4 and CXCR7 Is Protective in Acute Peritoneal Inflammation.Frontiers in immunology · 2020Article
- SDF-1α promotes repair of myocardial ischemic necrosis zones in rats.International journal of clinical and experimental pathology · 2019Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Restoration of the epithelial barrier following acute lung injury is critical for recovery of lung homeostasis. After injury, alveolar type II epithelial (ATII) cells spread and migrate to cover the denuded surface and, eventually, proliferate and differentiate into type I cells. The chemokine CXCL12, also known as stromal cell-derived factor 1α, has well-recognized roles in organogenesis, hematopoiesis, and immune responses through its binding to the chemokine receptor CXCR4. While CXCL12/CXCR4 signaling is known to be important in immune cell migration, the role of this chemokine-receptor interaction has not been studied in alveolar epithelial repair mechanisms. In this study, we demonstrated that secretion of CXCL12 was increased in the bronchoalveolar lavage of rats ventilated with an injurious tidal volume (25 ml/kg). We also found that CXCL12 secretion was increased by primary rat ATII cells and a mouse alveolar epithelial (MLE12) cell line following scratch wounding and that both types of cells express CXCR4. CXCL12 significantly increased ATII cell migration in a scratch-wound assay. When we treated cells with a specific antagonist for CXCR4, AMD-3100, cell migration was significantly inhibited. Knockdown of CXCR4 by short hairpin RNA (shRNA) caused decreased cell migration compared with cells expressing a nonspecific shRNA. Treatment with AMD-3100 decreased matrix metalloproteinase-14 expression, increased tissue inhibitor of metalloproteinase-3 expression, decreased matrix metalloproteinase-2 activity, and prevented CXCL12-induced Rac1 activation. Similar results were obtained with shRNA knockdown of CXCR4. These findings may help identify a therapeutic target for augmenting epithelial repair following acute lung injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.