ArticleTranslational research : the journal of laboratory and clinical medicine2017
Parkin regulates lipopolysaccharide-induced proinflammatory responses in acute lung injury.
Article in Translational research : the journal of laboratory and clinical medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 44 citations in OpenAlex.
- Article
- Advances in understanding mitophagy's role in lung injury.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2026Review
- Activation of USP30 Disrupts Endothelial Cell Function and Aggravates Acute Lung Injury Through Regulating the S-Adenosylmethionine Cycle.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Autophagy: a double-edged sword in ischemia-reperfusion injury.Cellular & molecular biology letters · 2025Review
- The Role of Ubiquitin-Proteasome System (UPS) in Asthma Pathology.Journal of asthma and allergy · 2025Review
- Regulation of the NLRP3 inflammasome by autophagy and mitophagy.Immunological reviews · 2025Review
- Parkin deficiency aggravates inflammation-induced acute lung injury by promoting necroptosis in alveolar type II cells.Chinese medical journal pulmonary and critical care medicine · 2024Article
- Inflammatory Intracellular Signaling in Neurons Is Influenced by Glial Soluble Factors in iPSC-Based Cell Model ofInternational journal of molecular sciences · 2024Article
- ApoE4 dysregulation incites depressive symptoms and mitochondrial impairments in mice.Journal of cellular and molecular medicine · 2024Article
- Parkin Promotes Airway Inflammatory Response to Interferon Gamma.Biomedicines · 2023Article
- The mitophagy pathway and its implications in human diseases.Signal transduction and targeted therapy · 2023Review
- Dysfunction in parkin aggravates inflammatory bone erosion by reinforcing osteoclast activity.Cell & bioscience · 2023Article
- Xiaochaihu Decoction Treatment of Chicken Colibacillosis by Improving Pulmonary Inflammation and Systemic Inflammation.Pathogens (Basel, Switzerland) · 2022Article
- Ibrutinib Prevents Acute Lung Injury via Multi-Targeting BTK, FLT3 and EGFR in Mice.International journal of molecular sciences · 2022Article
- Cortactin in Lung Cell Function and Disease.International journal of molecular sciences · 2022Review
- Molecular Perspectives of Mitophagy in Myocardial Stress: Pathophysiology and Therapeutic Targets.Frontiers in physiology · 2021Review
- Marrow-derived mesenchymal stem cells regulate the inflammatory response and repair alveolar type II epithelial cells in acute lung injury of rats.The Journal of international medical research · 2020Article
- Bcl-2 Proteins Regulate Mitophagy in Lipopolysaccharide-Induced Acute Lung Injury via PINK1/Parkin Signaling Pathway.Oxidative medicine and cellular longevity · 2020Article
- Loss of Microglial Parkin Inhibits Necroptosis and Contributes to Neuroinflammation.Molecular neurobiology · 2019Article
- Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The acute respiratory distress syndrome (ARDS) is a serious condition resulting from direct or indirect lung injury that is associated with high mortality and morbidity. A key biological event in the pathogenesis of the acute lung injury (ALI) that causes acute respiratory distress syndrome is activation of the lung endothelium cells (ECs), which is triggered by a variety of inflammatory insults leading to barrier disruption and excessive accumulation of neutrophils. Recently, we demonstrated that imatinib protects against lipopolysaccharide (LPS)-induced EC activation by inhibiting c-Abl kinase. In the present study, we explored the role of parkin, a novel c-Abl substrate, in ALI. Parkin is an E3 ubiquitin ligase originally characterized in the pathogenesis of Parkinson disease; however, its potential role in acute inflammatory processes and lung EC function remains largely unknown. Using parkin deficient (PARK2-/-) mice, we now demonstrate that parkin mediates LPS-induced ALI. After LPS, PARK2-/- mice have reduced total protein and cell levels in bronchoalveolar lavage (BAL) compared to wild type. Moreover, in LPS-treated PARK2-/- lungs, the sequestration and activation of neutrophils and release of inflammatory cytokines (interleukin 6 [IL-6], tumor necrosis factor alpha [TNF-α]) are significantly reduced. The BAL levels of soluble VCAM-1 and ICAM-1 are also decreased in LPS-treated PARK2-/- mice compared to wild type. In cultured human lung endothelial cells, downregulation of parkin by small interfering RNA decreases LPS-induced VCAM-1 expression, IL-8 and IL-6 secretion, and NF-kB phosphorylation. These results suggest a previously unidentified role of parkin in mediating endotoxin-induced endothelial proinflammatory signaling and indicate that it may play a critical role in acute inflammation.
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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.