ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2013
Lung endothelial HO-1 targeting in vivo using lentiviral miRNA regulates apoptosis and autophagy during oxidant injury.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 47 citations in OpenAlex.
- Neutrophil CD14 is a driver and a therapeutic target for deep vein thrombosis.Blood advances · 2026Article
- Epidermal growth factor receptor regulates Beclin-1 in hyperoxic acute lung injury.BMJ open respiratory research · 2026Article
- Review
- Upregulating carnitine palmitoyltransferase 1 attenuates hyperoxia-induced endothelial cell dysfunction and persistent lung injury.Respiratory research · 2022Article
- Sex differences and altered mitophagy in experimental pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Epidermal Growth Factor Receptor Inhibition Is Protective in Hyperoxia-Induced Lung Injury.Oxidative medicine and cellular longevity · 2022Article
- Genetic Delivery and Gene Therapy in Pulmonary Hypertension.International journal of molecular sciences · 2021Review
- Gene Therapy for Acute Respiratory Distress Syndrome.Frontiers in physiology · 2021Review
- Endosomes and Autophagy: Regulators of Pulmonary Endothelial Cell Homeostasis in Health and Disease.Antioxidants & redox signaling · 2019Review
- Endothelial toll-like receptor 4 maintains lung integrity via epigenetic suppression of p16Aging cell · 2019Article
- Fatty Acid Oxidation Protects against Hyperoxia-induced Endothelial Cell Apoptosis and Lung Injury in Neonatal Mice.American journal of respiratory cell and molecular biology · 2019Article
- Endothelial Stanniocalcin 1 Maintains Mitochondrial Bioenergetics and Prevents Oxidant-Induced Lung Injury via Toll-Like Receptor 4.Antioxidants & redox signaling · 2019Article
- Review
- Effect of Soluble Epoxide Hydrolase in Hyperoxic Acute Lung Injury in Mice.Inflammation · 2018Article
- Akap1 genetic deletion increases the severity of hyperoxia-induced acute lung injury in mice.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Impairment of an Endothelial NADCell · 2018Article
- Could Heme Oxygenase-1 Be a New Target for Therapeutic Intervention in Malaria-Associated Acute Lung Injury/Acute Respiratory Distress Syndrome?Frontiers in cellular and infection microbiology · 2018Review
- Effects of heme oxygenase-1 recombinant Lactococcus lactis on the intestinal barrier of hemorrhagic shock rats.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2017Article
- SH2 Domain-Containing Phosphatase-2 Is a Novel Antifibrotic Regulator in Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2017Article
- Inhibition of Regulatory-Associated Protein of Mechanistic Target of Rapamycin Prevents Hyperoxia-Induced Lung Injury by Enhancing Autophagy and Reducing Apoptosis in Neonatal Mice.American journal of respiratory cell and molecular biology · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The lung endothelium is a major target for inflammatory and oxidative stress. Heme oxygenase-1 (HO-1) induction is a crucial defense mechanism during oxidant challenges, such as hyperoxia. The role of lung endothelial HO-1 during hyperoxia in vivo is not well defined. We engineered lentiviral vectors with microRNA (miRNA) sequences controlled by vascular endothelium cadherin (VE-cad) to study the specific role of lung endothelial HO-1. Wild-type (WT) murine lung endothelial cells (MLECs) or WT mice were treated with lentivirus and exposed to hyperoxia (95% oxygen). We detected HO-1 knockdown (∼55%) specifically in the lung endothelium. MLECs and lungs showed approximately a 2-fold increase in apoptosis and ROS generation after HO-1 silencing. We also demonstrate for the first time that silencing endothelial HO-1 has the same effect on lung injury and survival as silencing HO-1 in multiple lung cell types and that HO-1 regulates caspase 3 activation and autophagy in endothelium during hyperoxia. These studies demonstrate the utility of endothelial-targeted gene silencing in vivo using lentiviral miRNA constructs to assess gene function and that endothelial HO-1 is an important determinant of survival during hyperoxia.
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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.