The effects of tongdujianbu particle treatment on matrix metallopeptidase 9 (MMP-9), tissue inhibitor of metalloproteinase (TIMP)-1, and transformation growth factor (TGF)-β1 expression in a rat model of spinal core injury

2012 ◽  
Vol 6 (16) ◽  
Author(s):  
Yi Luo
2020 ◽  
Vol 42 (3) ◽  
pp. 264-269
Author(s):  
Ryuki Matsuura ◽  
Shin-ichiro Hamano ◽  
Atsuro Daida ◽  
Hazuki Nonoyama ◽  
Jun Kubota ◽  
...  

2005 ◽  
Vol 288 (2) ◽  
pp. C435-C442 ◽  
Author(s):  
XiuXia Zhou ◽  
John B. Trudeau ◽  
Kathryn J. Schoonover ◽  
Jessica I. Lundin ◽  
Steve M. Barnes ◽  
...  

Tissue inhibitor of metalloproteinase (TIMP)-1 is a potent inhibitor of activated matrix metalloproteinases (MMPs) such as gelatinases and collagenases. TIMP-1 is induced by transforming growth factor-β1 (TGF-β1), but details regarding signaling pathways remain unclear. T-helper-2 cytokines also have profibrotic properties and can interact with TGF-β. In the present study, we examined the effects of interleukin (IL)-13 (2,500 pM) on TGF-β1 (200 pM)-induced expression of TIMP-1 mRNA and protein in primary human airway fibroblasts obtained from 57 human subjects. IL-13 alone had no effect on TIMP-1 mRNA or protein expression. However, IL-13 synergistically augmented TGF-β1-induced TIMP-1 mRNA and protein expression ( P < 0.001 vs. TGF-β1 alone). The upregulation of TIMP-1 by the combination of TGF-β1 and IL-13 involved increased transcription, with little effect on mRNA stabilization. Initial exploration of the pathways leading to the synergy determined that activation of the phosphatidylinositol 3-kinase (PI3K)-Akt pathway by IL-13 may have a negative effect on TIMP-1 production. The specific PI3K inhibitor LY-294002 in the presence of TGF-β1, IL-13, or the combination of the two caused significant increases in TIMP-1 mRNA expression, while LY-294002 increased TIMP-1 protein levels in the presence of IL-13 alone. These results suggest that IL-13 augments TGF-β1-induced profibrotic responses at both the mRNA and protein levels. Although IL-13 induced activation of PI3K-Akt, the activation did not contribute to the synergy observed with TGF-β1 plus IL-13 in TIMP-1 expression and in fact may dampen it. The mechanisms behind the synergy remain to be determined.


2021 ◽  
Vol 20 (9) ◽  
pp. 1855-1860
Author(s):  
Leibo Wang ◽  
Jianhua He ◽  
Ketao Xu ◽  
Weichao Zhu ◽  
Ketao Xu

Purpose: To investigate the differential expressions of transforming growth factor-β1 (TGF-β1), hypoxia inductive factor-1 (HIF-1), vascular endothelial growth factor (VEGF), α-smooth muscle protein (α-SMA) and E-cadherin in renal tissues of neonatal rat model of hydronephrosis.Methods: The neonatal rats (90) were randomly divided into sham group and model group. The rats in the model group were further divided into two subgroups: week 1 and week 12 after relief of obstruction, with 30 rats in each group. Six rats were taken from each group for the determination of renal histopathological changes. Levels of TGF-β1, HIF-1, VEGF, α-SMA and E-cadherin in renal tissues were compared for different pathological grades and at different time points of obstruction relief.Results: With increase in Elder grade, the concentrations of TGF-β1, HIF-1, VEGF and α-SMA in renal tissues of hydronephrosis neonatal rats were gradually increased, while the expression level of Ecadherin gradually decreased (p < 0.05). However, the concentrations of TGF-β1, HIF-1, VEGF and α-SMA in renal tissues were significantly reduced, while the expression level of E-adherin was upregulated with time after relief of obstruction (p < 0.05).Conclusion: These findings are of great significance in determining the degree of kidney injury and recovery, and for the development of drugs for the treatment of renal injury.


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