Toll-Like Receptor 4 Promotes NO Synthesis by Upregulating GCHI Expression under Oxidative Stress Conditions in Sheep MonocytesMacrophages
المؤلفون المشاركون
Deng, Shoulong
Yu, Kun
Zhang, Baolu
Yao, Yuchang
Wang, Zhixian
Zhang, Jinlong
Zhang, Xiaosheng
Liu, Guoshi
Li, Ning
Liu, Yixun
Lian, Zhengxing
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2015، العدد 2015 (31 ديسمبر/كانون الأول 2015)، ص ص. 1-11، 11ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2015-10-20
دولة النشر
مصر
عدد الصفحات
11
التخصصات الرئيسية
الملخص EN
Many groups of Gram-negative bacteria cause diseases that are harmful to sheep.
Toll-like receptor 4 (TLR4), which is critical for detecting Gram-negative bacteria by the innate immune system, is activated by lipopolysaccharide (LPS) to initiate inflammatory responses and oxidative stress.
Oxidation intermediates are essential activators of oxidative stress, as low levels of free radicals form a stressful oxidative environment that can clear invading pathogens.
NO is an oxidation intermediate and its generation is regulated by nitric oxide synthase (iNOS).
Guanosine triphosphate cyclohydrolase (GCHI) is the rate-limiting enzyme for tetrahydrobiopterin (BH4) synthesis, which is essential for the production of inducible iNOS.
Previously, we made vectors to overexpress the sheep TLR4 gene.
Herein, first generation (G1) of transgenic sheep was stimulated with LPS in vivo and in vitro, and oxidative stress and GCHI expression were investigated.
Oxidative injury caused by TLR4 overexpression was tightly regulated in tissues.
However, the transgenic (Tg) group still secreted nitric oxide (NO) when an iNOS inhibitor was added.
Furthermore, GCHI expression remained upregulated in both serum and monocytes/macrophages.
Thus, overexpression of TLR4 in transgenic sheep might accelerate the clearance of invading microbes through NO generation following LPS stimulation.
Additionally, TLR4 overexpression also enhances GCHI activation.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Deng, Shoulong& Yu, Kun& Zhang, Baolu& Yao, Yuchang& Wang, Zhixian& Zhang, Jinlong…[et al.]. 2015. Toll-Like Receptor 4 Promotes NO Synthesis by Upregulating GCHI Expression under Oxidative Stress Conditions in Sheep MonocytesMacrophages. Oxidative Medicine and Cellular Longevity،Vol. 2015, no. 2015, pp.1-11.
https://search.emarefa.net/detail/BIM-1075601
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Deng, Shoulong…[et al.]. Toll-Like Receptor 4 Promotes NO Synthesis by Upregulating GCHI Expression under Oxidative Stress Conditions in Sheep MonocytesMacrophages. Oxidative Medicine and Cellular Longevity No. 2015 (2015), pp.1-11.
https://search.emarefa.net/detail/BIM-1075601
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Deng, Shoulong& Yu, Kun& Zhang, Baolu& Yao, Yuchang& Wang, Zhixian& Zhang, Jinlong…[et al.]. Toll-Like Receptor 4 Promotes NO Synthesis by Upregulating GCHI Expression under Oxidative Stress Conditions in Sheep MonocytesMacrophages. Oxidative Medicine and Cellular Longevity. 2015. Vol. 2015, no. 2015, pp.1-11.
https://search.emarefa.net/detail/BIM-1075601
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1075601
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