Mechanism of Mechanical Trauma-Induced Extracellular Matrix Remodeling of Fibroblasts in Association with Nrf2ARE Signaling Suppression Mediating TGF-β1Smad3 Signaling Inhibition
المؤلفون المشاركون
Tang, Jianming
Min, Jie
Hu, Ming
Li, Yang
Hong, Li
Li, Bingshu
Liu, Cheng
Li, Qiannan
Wang, Linlin
Hong, Shasha
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2017، العدد 2017 (31 ديسمبر/كانون الأول 2017)، ص ص. 1-14، 14ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2017-10-03
دولة النشر
مصر
عدد الصفحات
14
التخصصات الرئيسية
الملخص EN
Stress urinary incontinence (SUI) is a common hygienic problem affecting the quality of women’s life worldwide.
In this research, we revealed the involvement and regulation of extracellular matrix (ECM) remodeling, oxidative damage, and TGF-β1 signaling in the pathological mechanisms of mechanical trauma-induced SUI.
We found that excessive mechanical strain significantly increased apoptosis rate, decreased cell viability and ECM production, and broke the balance of MMPs/TIMPs compared with the nonstrain control (NC) group.
The expression levels of TGFβ1, p-Smad3, Nrf2, GPx1, and CAT were downregulated, the production of ROS, 8-OHdG, 4-HNE, and MDA was increased, and the nuclear translocation of Smad2/3 was suppressed after 5333 μstrain’s treatment.
Both mTGF-β1 pretreatment and Nrf2 overexpression could reverse mechanical injury-induced TGFβ1/Smad3 signaling inhibition and ECM remodeling, whereas mTGF-β1 had no effect on Nrf2 expression.
Nrf2 overexpression significantly alleviated mechanical injury-induced ROS accumulation and oxidative damage; in contrast, Nrf2 silencing exhibited opposite effects.
Besides, vaginal distention- (VD-) induced in vivo SUI model was used to confirm the in vitro results; Nrf2 knockout aggravates mechanical trauma-induced LPP reduction, ECM remodeling, oxidative damage, and TGF-β1/Smad3 suppression in mice.
Therefore, we deduce that mechanical injury-induced ECM remodeling might be associated with Nrf2/ARE signaling suppression mediating TGF-β1/Smad3 signaling inhibition.
This might reflect a new molecular target for SUI researches.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Tang, Jianming& Li, Bingshu& Liu, Cheng& Li, Yang& Li, Qiannan& Wang, Linlin…[et al.]. 2017. Mechanism of Mechanical Trauma-Induced Extracellular Matrix Remodeling of Fibroblasts in Association with Nrf2ARE Signaling Suppression Mediating TGF-β1Smad3 Signaling Inhibition. Oxidative Medicine and Cellular Longevity،Vol. 2017, no. 2017, pp.1-14.
https://search.emarefa.net/detail/BIM-1196173
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Tang, Jianming…[et al.]. Mechanism of Mechanical Trauma-Induced Extracellular Matrix Remodeling of Fibroblasts in Association with Nrf2ARE Signaling Suppression Mediating TGF-β1Smad3 Signaling Inhibition. Oxidative Medicine and Cellular Longevity No. 2017 (2017), pp.1-14.
https://search.emarefa.net/detail/BIM-1196173
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Tang, Jianming& Li, Bingshu& Liu, Cheng& Li, Yang& Li, Qiannan& Wang, Linlin…[et al.]. Mechanism of Mechanical Trauma-Induced Extracellular Matrix Remodeling of Fibroblasts in Association with Nrf2ARE Signaling Suppression Mediating TGF-β1Smad3 Signaling Inhibition. Oxidative Medicine and Cellular Longevity. 2017. Vol. 2017, no. 2017, pp.1-14.
https://search.emarefa.net/detail/BIM-1196173
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1196173
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