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Mechanism of Mechanical Trauma-Induced Extracellular Matrix Remodeling of Fibroblasts in Association with Nrf2ARE Signaling Suppression Mediating TGF-β1Smad3 Signaling Inhibition
Joint Authors
Tang, Jianming
Min, Jie
Hu, Ming
Li, Yang
Hong, Li
Li, Bingshu
Liu, Cheng
Li, Qiannan
Wang, Linlin
Hong, Shasha
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2017, Issue 2017 (31 Dec. 2017), pp.1-14, 14 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2017-10-03
Country of Publication
Egypt
No. of Pages
14
Main Subjects
Abstract 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.
American Psychological Association (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
Modern Language Association (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
American Medical Association (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
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1196173