ArticleAmerican journal of respiratory cell and molecular biology2012
Cigarette smoke-induced CXCR3 receptor up-regulation mediates endothelial apoptosis.
Article in American journal of respiratory cell and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
- Y-Chromosome Gene,American journal of respiratory and critical care medicine · 2022Article
- Polymorphisms in CXCR3 ligands predict early CXCL9 recovery and severe chronic GVHD.Blood cancer journal · 2021Article
- EMAPII: A Key Player in HIV-Nef-induced Pulmonary Vasculopathy.American journal of respiratory cell and molecular biology · 2019Article
- HIV-Nef Protein Persists in the Lungs of Aviremic Patients with HIV and Induces Endothelial Cell Death.American journal of respiratory cell and molecular biology · 2019Article
- Subcutaneous administration of neutralizing antibodies to endothelial monocyte-activating protein II attenuates cigarette smoke-induced lung injury in mice.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Endothelial cells are a source of Nestin expression in Pulmonary Arterial Hypertension.PloS one · 2019Article
- EMAPII Monoclonal Antibody Ameliorates Influenza A Virus-Induced Lung Injury.Molecular therapy : the journal of the American Society of Gene Therapy · 2018Article
- Effects of cigarette smoke on pulmonary endothelial cells.American journal of physiology. Lung cellular and molecular physiology · 2018Review
- Pulmonary Microvascular Blood Flow in Mild Chronic Obstructive Pulmonary Disease and Emphysema. The MESA COPD Study.American journal of respiratory and critical care medicine · 2015Article
- Overexpression of interleukin-8 receptor 2 (IL-8R2) indicates better prognosis in esophageal adenocarcinoma and squamous cell carcinoma procession.Medical oncology (Northwood, London, England) · 2014Article
- Activation of p38-MAPK by CXCL4/CXCR3 axis contributes to p53-dependent intestinal apoptosis initiated by 5-fluorouracil.Cancer biology & therapy · 2014Article
- HIV envelope protein gp120-induced apoptosis in lung microvascular endothelial cells by concerted upregulation of EMAP II and its receptor, CXCR3.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- Article
- Inflammatory Markers of the Systemic Capillary Leak Syndrome (Clarkson Disease).Journal of clinical & cellular immunology · 2014Article
- Nonclassically Secreted Regulators of Angiogenesis.Angiology: open access · 2013Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Endothelial monocyte-activating polypeptide II (EMAP II) and interferon-inducible protein (IP)-10 are proinflammatory mediators, which in addition to their chemokine activities, selectively induce apoptosis in endothelial cells and are up-regulated in the lungs of cigarette smoke-exposed humans. Previously, we showed that EMAP II is an essential mediator of cigarette smoke-induced lung emphysema in mice linking endothelial cell apoptosis with inflammation. Here we addressed the role of the CXCR3 receptor in EMAP II-induced and IP-10-induced apoptosis in endothelial cells and its regulation by cigarette smoke. We found that both neutralizing antibodies and small inhibitory RNA to CXCR3 abrogated EMAP II-induced and IP-10-induced endothelial caspase-3 activation and DNA fragmentation. CXCR3 receptor surface expression in human lung microvascular endothelial cells and in lung tissue endothelium was up-regulated by exposure to cigarette smoke. In tissue culture conditions, EMAP II-induced and IP-10-induced apoptosis was enhanced by preincubation with cigarette smoke extract. Interestingly, serum starvation also induced CXCR3 up-regulation and enhanced EMAP II-induced endothelial apoptosis. Signal transduction via p38 mitogen-activated protein kinase activation was essential for CXCR3-induced cell death, but not for CXCR3 receptor up-regulation by cigarette smoke. In turn, protein nitration was required for CXCR3 receptor up-regulation by cigarette smoke and consequently for subsequent CXCR3-induced cell death. In conclusion, the concerted up-regulation of proinflammatory EMAP II, IP-10, and CXCR3 by cigarette smoke could sustain a cascade of cell death that may promote the alveolar tissue loss noted in human emphysema.
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