Academic Journal

Role of Paraoxonase 2 in Airway Epithelial Response to Oxidant Stress

التفاصيل البيبلوغرافية
العنوان: Role of Paraoxonase 2 in Airway Epithelial Response to Oxidant Stress
المؤلفون: Matthew S. McCravy, Zhonghui Yang, Jaime Cyphert-Daly, Zachary R. Healy, Aaron V. Vose, Haein R. Kim, Julia K. L. Walker, Robert M. Tighe, Heath G. Gasier, Jennifer L. Ingram, Loretta G. Que
المصدر: Antioxidants, Vol 13, Iss 11, p 1333 (2024)
بيانات النشر: MDPI AG, 2024.
سنة النشر: 2024
المجموعة: LCC:Therapeutics. Pharmacology
مصطلحات موضوعية: asthma, ozone, paraoxonase, oxidant stress, mitochondria, Therapeutics. Pharmacology, RM1-950
الوصف: Asthma is a widespread chronic lung disease characterized by airway inflammation and hyperresponsiveness. This airway inflammation is classified by either the presence (T2-high) or absence (T2-low) of high levels of eosinophils. Because most therapies for asthma target eosinophils and related pathways, treatment options for T2-low disease are limited. New pathophysiologic targets are needed. Oxidant stress is a common feature of T2-low disease. Airway epithelial expression of the antioxidant enzyme Paraoxonase 2 (PON2) is decreased in a well-recognized population of people with T2-low asthma and people with obesity and asthma. As a potential mechanism of increased oxidant stress, we measured the role of PON2 in lung oxidant responses using an environmentally relevant in vivo murine oxidant exposure (i.e., ozone) and in vitro studies with an immortalized human airway epithelial cell line BEAS-2B. Pon2-deficient (Pon2−/−) mice developed increased airway hyper-responsiveness compared to wild-type controls. Despite reduced alveolar macrophage influx, Pon2−/− mice exhibited increased nitrite production. In human airway epithelial cells incubated with hydrogen peroxide, PON2 knockdown (PON2KD) decreased mitochondrial function and inner mitochondrial membrane potential. These findings suggest that PON2 functions in defending against airway epithelial oxidant stress. Further studies are needed to elucidate the mechanisms linking PON2, oxidant stress, and asthma pathogenesis.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 2076-3921
Relation: https://www.mdpi.com/2076-3921/13/11/1333; https://doaj.org/toc/2076-3921
DOI: 10.3390/antiox13111333
URL الوصول: https://doaj.org/article/cd208752425c459a965a3e74f5d926bf
رقم الانضمام: edsdoj.208752425c459a965a3e74f5d926bf
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:20763921
DOI:10.3390/antiox13111333