ArticleAnnals of surgery2018
Molecular Characterization of Hypoxic Alveolar Epithelial Cells After Lung Contusion Indicates an Important Role for HIF-1α.
Article in Annals of surgery, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 21 citations in OpenAlex.
- Fraxinellone mitigates acute lung injury by targeting HIF-1α to suppress pyroptosis and inflammation.Frontiers in immunology · 2026Article
- Interplay of HIF-1α, SMAD2, and VEGF signaling in hypoxic renal environments: impact on macrophage polarization and renoprotection.Renal failure · 2025Article
- Experimental study of a novel mouse model of tibial shaft fracture combined with blunt chest trauma.Animal models and experimental medicine · 2025Article
- Expression and Regulation of Hypoxia-Inducible Factor Signalling in Acute Lung Inflammation.Cells · 2024Review
- The HIF-1α/EGF/EGFR Signaling Pathway Facilitates the Proliferation of Yak Alveolar Type II Epithelial Cells in Hypoxic Conditions.International journal of molecular sciences · 2024Article
- Role of succinate in airway epithelial cell regulation following traumatic lung injury.JCI insight · 2023Article
- The Intriguing Role of Hypoxia-Inducible Factor in Myocardial Ischemia and Reperfusion: A Comprehensive Review.Journal of cardiovascular development and disease · 2023Review
- Hypoxia-Inducible Factor 1α and Its Role in Lung Injury: Adaptive or Maladaptive.Inflammation · 2023Review
- Hypoxia-inducible factor (HIF)-1α-induced regulation of lung injury in pulmonary aspiration is mediated through NF-kB.FASEB bioAdvances · 2022Article
- Characterization of circRNA-miRNA-mRNA networks regulating oxygen utilization in type II alveolar epithelial cells of Tibetan pigs.Frontiers in molecular biosciences · 2022Article
- Alternative splicing signature of alveolar type II epithelial cells of Tibetan pigs under hypoxia-induced.Frontiers in veterinary science · 2022Article
- Integrative Analysis of the lncRNA-Associated ceRNA Regulatory Network Response to Hypoxia in Alveolar Type II Epithelial Cells of Tibetan Pigs.Frontiers in veterinary science · 2022Article
- COVID-19: imbalance of multiple systems during infection and importance of therapeutic choice and dosing of cardiac and anti-coagulant therapies.Molecular biology reports · 2021Review
- Regulating the immunosuppressive tumor microenvironment to enhance breast cancer immunotherapy using pH-responsive hybrid membrane-coated nanoparticles.Journal of nanobiotechnology · 2021Article
- TLR3 absence confers increased survival with improved macrophage activity against pneumonia.JCI insight · 2019Article
- Direct pulmonary delivery of solubilized curcumin reduces severity of lethal pneumonia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Hypoxia-Inducible Factor (HIF)-1α Promotes Inflammation and Injury Following Aspiration-Induced Lung Injury in Mice.Shock (Augusta, Ga.) · 2019Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTo understand the fate and regulation of hypoxic type II alveolar epithelial cells (AECs) after lung contusion (LC).
backgroundLC due to thoracic trauma is a major risk factor for the development of acute respiratory distress syndrome. AECs have recently been implicated as a primary driver of inflammation in LC. The main pathological consequence of LC is hypoxia, and a key mediator of adaptation to hypoxia is hypoxia-inducible factor (HIF)-1. We have recently published that HIF-1α is a major driver of acute inflammation after LC through type II AEC.
methodsLC was induced in wild-type mice (C57BL/6), luciferase-based hypoxia reporter mice (ODD-Luc), and HIF-1α conditional knockout mice. The degree of hypoxia was assessed using hypoxyprobe and in vivo imaging system. The fate of hypoxic AEC was evaluated by luciferase dual staining with caspases-3 and Ki-67, terminal deoxynucleotidyl transferase dUTP nick end labeling, and flow cytometry with ApoStat. NLRP-3 expression was determined by western blot. Laser capture microdissection was used to isolate AECs in vivo, and collected RNA was analyzed by Q-PCR for HIF-related pathways.
resultsGlobal hypoxia was present after LC, but hypoxic foci were not uniform. Hypoxic AECs preferentially undergo apoptosis. There were significant reductions in NLRP-3 in HIF-1α conditional knockout mice. The expression of proteins involved in HIF-related pathways and inflammasome activation were significantly increased in hypoxic AECs.
conclusionsThese are the first in vivo data to identify, isolate, and characterize hypoxic AECs. HIF-1α regulation through hypoxic AECs is critical to the initiation of acute inflammation after LC.
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