Total polysaccharide of Y upingfeng protects against bleomycin-induced pulmonary fibrosis via inhibiting transforming growth factor-β1-mediated type I collagen abnormal deposition in rats

2014 ◽  
Vol 66 (12) ◽  
pp. 1786-1795 ◽  
Author(s):  
Liang Xu ◽  
Liu-cheng Li ◽  
Ping Zhao ◽  
Lian-wen Qi ◽  
Ping Li ◽  
...  
Keyword(s):  
Growth Factor ◽  
Pulmonary Fibrosis ◽  
Type I Collagen ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Type I

scholarly journals Decreased MiR-30a promotes TGF-β1-mediated arachnoid fibrosis in post-hemorrhagic hydrocephalus

2020 ◽  
Vol 11 (1) ◽  
pp. 60-74
Author(s):  
Chaohong Zhan ◽  
Gelei Xiao ◽  
Xiangyang Zhang ◽  
Xiaoyu Chen ◽  
Zhiping Zhang ◽  
...  
Keyword(s):  
Growth Factor ◽  
Intraventricular Hemorrhage ◽  
Type I Collagen ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Ventricular System ◽  
Type I ◽  
Cerebral Ventricles ◽  
The Right ◽  
Tgf Β1

AbstractBackgroundFibrosis in the ventricular system is closely associated with post-hemorrhagic hydrocephalus (PHH). It is characterized by an expansion of the cerebral ventricles due to CSF accumulation following intraventricular hemorrhage (IVH). The activation of transforming growth factor-β1 (TGF-β1) may be involved in thrombin-induced arachnoid fibrosis.MethodsA rat model of PHH was established by injection of autologous non-anticoagulated blood from the right femoral artery into the lateral ventricles. Differential expression of miR-30a was detected in rat arachnoid cells by RNA sequencing. AP-1, c-Fos, and TRAF3IP2 were knocked down in primary arachnoid cells, and the degree of arachnoid fibrosis was assessed.ResultsDecreased expression of miR-30a and increased expression of TRAF3IP2, TGF-β1, and α-SMA were detected in the arachnoid cells of PHH rat. Besides, overexpression of miR-30a targets TRAF3IP2 mRNA 3′UTR and inhibits the expression of TRAF3IP2, TGF-β1, and α-SMA in the primary arachnoid cells. Furthermore, TRAF3IP2 activates AP-1 to promote arachnoid fibrosis. The content of type I collagen in the primary arachnoid cells was reduced after the silencing of AP-1 and TRAF3IP2.ConclusionsThis study identified a miR-30a-regulated mechanism of arachnoid fibrosis, suggesting a previously unrecognized contribution of miR-30a to the pathogenesis of fibrosis in the ventricular system. These results might provide a new target for the clinical diagnosis and treatment of PHH.

Sign in / Sign up

Export Citation Format

Share Document