Opposing Effects of Oxygen Regulation on Kallistatin Expression: Kallistatin as a Novel Mediator of Oxygen-Induced HIF-1-eNOS-NO Pathway
المؤلفون المشاركون
Chao, Julie
Guo, Youming
Li, Pengfei
Chao, Lee
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2017، العدد 2017 (31 ديسمبر/كانون الأول 2017)، ص ص. 1-8، 8ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2017-12-13
دولة النشر
مصر
عدد الصفحات
8
التخصصات الرئيسية
الملخص EN
Oxidative stress has both detrimental and beneficial effects.
Kallistatin, a key component of circulation, protects against vascular and organ injury.
Serum kallistatin levels are reduced in patients and animal models with hypertension, diabetes, obesity, and cancer.
Reduction of kallistatin levels is inversely associated with elevated thiobarbituric acid-reactive substance.
Kallistatin therapy attenuates oxidative stress and increases endothelial nitric oxide synthase (eNOS) and NO levels in animal models.
However, kallistatin administration increases reactive oxygen species formation in immune cells and bacterial killing activity in septic mice.
High oxygen inhibits kallistatin expression via activating the JNK-FOXO1 pathway in endothelial cells.
Conversely, mild oxygen/hyperoxia stimulates kallistatin, eNOS, and hypoxia-inducible factor-1 (HIF-1) expression in endothelial cells and in the kidney of normal mice.
Likewise, kallistatin stimulates eNOS and HIF-1, and kallistatin antisense RNA abolishes oxygen-induced eNOS and HIF-1 expression, indicating a role of kallistatin in mediating mild oxygen’s stimulation on antioxidant genes.
Protein kinase C (PKC) activation mediates HIF-1-induced eNOS synthesis in response to hyperoxia/exercise; thus, mild oxygen through PKC activation stimulates kallistatin-mediated HIF-1 and eNOS synthesis.
In summary, oxidative stress induces down- or upregulation of kallistatin expression, depending on oxygen concentration, and kallistatin plays a novel role in mediating oxygen/exercise-induced HIF-1-eNOS-NO pathway.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Chao, Julie& Guo, Youming& Li, Pengfei& Chao, Lee. 2017. Opposing Effects of Oxygen Regulation on Kallistatin Expression: Kallistatin as a Novel Mediator of Oxygen-Induced HIF-1-eNOS-NO Pathway. Oxidative Medicine and Cellular Longevity،Vol. 2017, no. 2017, pp.1-8.
https://search.emarefa.net/detail/BIM-1194927
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Chao, Julie…[et al.]. Opposing Effects of Oxygen Regulation on Kallistatin Expression: Kallistatin as a Novel Mediator of Oxygen-Induced HIF-1-eNOS-NO Pathway. Oxidative Medicine and Cellular Longevity No. 2017 (2017), pp.1-8.
https://search.emarefa.net/detail/BIM-1194927
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Chao, Julie& Guo, Youming& Li, Pengfei& Chao, Lee. Opposing Effects of Oxygen Regulation on Kallistatin Expression: Kallistatin as a Novel Mediator of Oxygen-Induced HIF-1-eNOS-NO Pathway. Oxidative Medicine and Cellular Longevity. 2017. Vol. 2017, no. 2017, pp.1-8.
https://search.emarefa.net/detail/BIM-1194927
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1194927
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
تقوم هذه الخدمة بالتحقق من التشابه أو الانتحال في الأبحاث والمقالات العلمية والأطروحات الجامعية والكتب والأبحاث باللغة العربية، وتحديد درجة التشابه أو أصالة الأعمال البحثية وحماية ملكيتها الفكرية. تعرف اكثر