دورية أكاديمية

MG53 preserves mitochondrial integrity of cardiomyocytes during ischemia reperfusion-induced oxidative stress

التفاصيل البيبلوغرافية
العنوان: MG53 preserves mitochondrial integrity of cardiomyocytes during ischemia reperfusion-induced oxidative stress
المؤلفون: Kristyn Gumpper-Fedus, Ki Ho Park, Hanley Ma, Xinyu Zhou, Zehua Bian, Karthikeyan Krishnamurthy, Matthew Sermersheim, Jingsong Zhou, Tao Tan, Lei Li, Jianxun Liu, Pei-Hui Lin, Hua Zhu, Jianjie Ma
المصدر: Redox Biology, Vol 54, Iss , Pp 102357- (2022)
بيانات النشر: Elsevier, 2022.
سنة النشر: 2022
المجموعة: LCC:Medicine (General)
LCC:Biology (General)
مصطلحات موضوعية: Cardioprotection, Mitophagy, Cell membrane repair, TRIM72, Myocardial infarction, Cardiolipin, Medicine (General), R5-920, Biology (General), QH301-705.5
الوصف: Ischemic injury to the heart induces mitochondrial dysfunction due to increasing oxidative stress. MG53, also known as TRIM72, is highly expressed in striated muscle, is secreted as a myokine after exercise, and is essential for repairing damaged plasma membrane of many tissues by interacting with the membrane lipid phosphatidylserine (PS). We hypothesized MG53 could preserve mitochondrial integrity after an ischemic event by binding to the mitochondrial-specific lipid, cardiolipin (CL), for mitochondria protection to prevent mitophagy. Fluorescent imaging and Western blotting experiments showed recombinant human MG53 (rhMG53) translocated to the mitochondria after ischemic injury in vivo and in vitro. Fluorescent imaging indicated rhMG53 treatment reduced superoxide generation in ex vivo and in vitro models. Lipid-binding assay indicated MG53 binds to CL. Transfecting cardiomyocytes with the mitochondria-targeted mt-mKeima showed inhibition of mitophagy after MG53 treatment. Overall, we show that rhMG53 treatment may preserve cardiac function by preserving mitochondria in cardiomyocytes. These findings suggest MG53's interactions with mitochondria could be an attractive avenue for developing MG53 as a targeted protein therapy for cardioprotection.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 2213-2317
Relation: http://www.sciencedirect.com/science/article/pii/S221323172200129X; https://doaj.org/toc/2213-2317
DOI: 10.1016/j.redox.2022.102357
URL الوصول: https://doaj.org/article/fc9de50b82074903baf28b9239dfefd1
رقم الأكسشن: edsdoj.fc9de50b82074903baf28b9239dfefd1
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:22132317
DOI:10.1016/j.redox.2022.102357