hCLOCK Causes Rho-Kinase-Mediated Endothelial Dysfunction and NF-κB-Mediated Inflammatory Responses
المؤلفون المشاركون
Tang, Xiao
Guo, Daqiao
Lin, Changpo
Shi, Zhenyu
Qian, Ruizhe
Fu, Weiguo
Liu, Jianjun
Li, Xu
Fan, Longhua
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2015، العدد 2015 (31 ديسمبر/كانون الأول 2015)، ص ص. 1-9، 9ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2015-10-25
دولة النشر
مصر
عدد الصفحات
9
التخصصات الرئيسية
الملخص EN
Background.
The human Circadian Locomotor Output Cycle protein Kaput (CLOCK) gene was originally discovered as a regulator of essential human daily rhythms.
This seemingly innocuous gene was then found to be associated with a multitude of human malignancies, via several biochemical pathways.
We aimed to further investigate the role of hCLOCK in the hypoxia-oxidative stress response system at the biochemical level.
Methods.
Expression levels of Rho GTPases were measured in normoxic and hypoxic states.
The effect of hCLOCK on the hypoxic response was evaluated with the use of a retroviral shRNA vector system, a Rho inhibitor, and a ROS scavenger by analyzing expression levels of hCLOCK, Rho GTPases, and NF-κB pathway effectors.
Finally, in vitro ROS production and tube formation in HUVECs were assessed.
Results.
Hypoxia induces ROS production via hCLOCK.
hCLOCK activates the RhoA and NF-κB signaling pathways.
Conversely, inhibition of hCLOCK deactivates these pathways.
Furthermore, inhibition of RhoA or decreased levels of ROS attenuate these pathways, but inhibition of RhoA does not lead to decreased levels of ROS.
Overall findings show that hypoxia increases the expression of hCLOCK, which leads to ROS production, which then activates the RhoA and NF-κB pathways.
Conclusion.
Our findings suggest that hypoxic states induce vascular oxidative damage and inflammation via hCLOCK-mediated production of ROS, with subsequent activation of the RhoA and NF-κB pathways.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Tang, Xiao& Guo, Daqiao& Lin, Changpo& Shi, Zhenyu& Qian, Ruizhe& Fu, Weiguo…[et al.]. 2015. hCLOCK Causes Rho-Kinase-Mediated Endothelial Dysfunction and NF-κB-Mediated Inflammatory Responses. Oxidative Medicine and Cellular Longevity،Vol. 2015, no. 2015, pp.1-9.
https://search.emarefa.net/detail/BIM-1075731
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Tang, Xiao…[et al.]. hCLOCK Causes Rho-Kinase-Mediated Endothelial Dysfunction and NF-κB-Mediated Inflammatory Responses. Oxidative Medicine and Cellular Longevity No. 2015 (2015), pp.1-9.
https://search.emarefa.net/detail/BIM-1075731
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Tang, Xiao& Guo, Daqiao& Lin, Changpo& Shi, Zhenyu& Qian, Ruizhe& Fu, Weiguo…[et al.]. hCLOCK Causes Rho-Kinase-Mediated Endothelial Dysfunction and NF-κB-Mediated Inflammatory Responses. Oxidative Medicine and Cellular Longevity. 2015. Vol. 2015, no. 2015, pp.1-9.
https://search.emarefa.net/detail/BIM-1075731
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1075731
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