Antifibrotic activity of anisodaminein vivois associated with changed intrahepatic levels of matrix metalloproteinase-2 and its inhibitor tissue inhibitors of metalloproteinases-2 and transforming growth factor β1 in rats with carbon tetrachloride-induced liver injury

2009 ◽  
Vol 24 (6) ◽  
pp. 1070-1076 ◽  
Author(s):  
Lin Luo ◽  
Ailing Zhou
Keyword(s):  
Carbon Tetrachloride ◽  
Growth Factor ◽  
Liver Injury ◽  
Matrix Metalloproteinase ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Tissue Inhibitors Of Metalloproteinases ◽  
Matrix Metalloproteinase 2 ◽  
Tissue Inhibitors

scholarly journals Thrombospondin 1 does not activate transforming growth factor β1 in a chemically defined system or in smooth-muscle-cell cultures

2000 ◽  
Vol 350 (1) ◽  
pp. 291-298 ◽  
Author(s):  
David J. GRAINGER ◽  
Emma K. FROW
Keyword(s):  
Cell Culture ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Matrix Metalloproteinase ◽  
Smooth Muscle Cell ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Matrix Metalloproteinase 2 ◽  
Tgf Β1

The cytokine transforming growth factor β1 (TGF-β1) is secreted in a latent form that has no known biological activity. The conversion of latent TGF-β1 into its biologically active 25kDa form is thought to be an important step in the regulation of TGF-β activity both in cell culture and in vivo. Thrombospondin (TSP)-1, a 360kDa platelet α-granule and extracellular matrix protein, has been shown to participate in TGF-β1 activation. We have used a chemically defined system to examine the mechanism of TSP-1-mediated TGF-β1 activation. However, the addition of two different preparations of TSP-1 to recombinant small latent TGF-β1 in the test tube resulted in only a very small increase in the proportion of the TGF-β1 able to bind to the TGF-β type II receptor: from 0.1% to a maximum of 0.4%. This small effect was not specific for TSP-1: matrix metalloproteinase 2, tissue inhibitor of matrix metalloproteinase 2 and active plasminogen activator inhibitor 1, but not transglutaminase, human serum albumin or immunoglobulin, had quantitatively similar effects on latent TGF-β1. Furthermore, no change in the activity associated with small latent TGF-β1 was noted in either mink lung epithelial cell or rat aortic smooth-muscle cell culture systems in the presence of TSP-1 (or TSP-1-derived peptides). We conclude that TSP-1, either alone or in the presence of cultured smooth-muscle cells (a cell type known to activate latent TGF-β in vitro and in vivo) is unable to activate latent TGF-β1. Any TSP-mediated activation of TGF-β1 must depend on additional factor(s) not present in our systems.

Transforming Growth Factor-β1 Bioassay Involving Matrix Metalloproteinase-2 Induction

2010 ◽  
Vol 30 (9) ◽  
pp. 667-672 ◽  
Author(s):  
Gi-Hyun Kim ◽  
So-Young Kang ◽  
Ho-Jung Kwak ◽  
Kyung-Min Baek ◽  
Seung-Hwa Hong ◽  
...  
Keyword(s):  
Growth Factor ◽  
Matrix Metalloproteinase ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Matrix Metalloproteinase 2

scholarly journals Macrophage-Derived Legumain Promotes Pulmonary Hypertension by Activating the MMP (Matrix Metalloproteinase)-2/TGF (Transforming Growth Factor)-β1 Signaling

2019 ◽  
Vol 39 (4) ◽  
Author(s):  
Peiyuan Bai ◽  
Luheng Lyu ◽  
Tingting Yu ◽  
Caojian Zuo ◽  
Jie Fu ◽  
...  
Keyword(s):  
Growth Factor ◽  
Matrix Metalloproteinase ◽  
Right Ventricular ◽  
Transforming Growth Factor ◽  
Cysteine Proteinase ◽  
Active Form ◽  
Transforming Growth Factor Β1 ◽  
Left Ventricular ◽  
Matrix Metalloproteinase 2 ◽  
Ventricular Wall

Objective— Macrophages participate in the pathogenesis of pulmonary arterial hypertension (PAH). Lgmn (Legumain), a newly discovered cysteine proteinase belonging to the C13 peptidase family, is primarily expressed in macrophages; however, its roles in PAH remain unknown. Approach and Results— Herein, Lgmn was upregulated in lung tissues of PAH mice subjected to hypoxia plus SU5416 and PAH rats challenged with monocrotaline. Global Lgmn ablation and macrophage-specific ablation alleviated PAH compared with wild-type mice, evident from a reduction in right ventricular systolic pressure, the ratio of the right ventricular wall to the left ventricular wall plus the septum, the pulmonary vascular media thickness, and pulmonary vascular muscularization. Increased expression of ECM (extracellular matrix) proteins was correlated with MMP (matrix metalloproteinase)-2 activation and TGF (transforming growth factor)-β1 signaling in the PAs. Although Lgmn did not affect inflammatory cell infiltration and PA smooth muscle cell proliferation, it drove increased the synthesis of ECM proteins via MMP-2 activation. MMP-2 hydrolyzed the TGF-β1 precursor to the active form. An Lgmn-specific inhibitor markedly ameliorated PAH. Clinically, serum Lgmn levels were closely associated with the severity of idiopathic PAH. Conclusions— Our results indicate that Lgmn inhibition could be an effective strategy for preventing or delaying PAH.

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