scholarly journals Membrane-Type 1 Matrix Metalloproteinase Downregulates Fibroblast Growth Factor-2 Binding to the Cell Surface and Intracellular Signaling

2014 ◽  
Vol 230 (2) ◽  
pp. 366-377 ◽  
Author(s):  
Evelyne Tassone ◽  
Cristina Valacca ◽  
Paolo Mignatti
Keyword(s):  
Growth Factor ◽  
Cell Surface ◽  
Matrix Metalloproteinase ◽  
Fibroblast Growth Factor ◽  
Intracellular Signaling ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Membrane Type

Fibroblast Growth Factor-2 Mediates Angiotensin Ii-Induced Cardiac Hypertrophy in Renovascular Hypertension

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 683-683
Author(s):  
Corinne Pellieux ◽  
Alessandro Foletti ◽  
Thercse Sauthier ◽  
Aubert Jean-Francois ◽  
Beermann Friedrich ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Growth Factor ◽  
Cardiac Hypertrophy ◽  
Fibroblast Growth Factor ◽  
Renovascular Hypertension ◽  
Intracellular Signaling ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Jnk Activation

29 In renovascular hypertension, angiotensin II leads to an elevation of blood pressure and to cardiac hypertrophy. The fibroblast growth factor-2 (FGF-2) has been implicated in cardiomyocyte growth. Therefore, we investigated whether FGF-2 could control the development of angiotensin II-induced cardiac hypertrophy. Mice deficient for the expression of FGF-2 were created, and the role of FGF-2 was investigated in the two kidney-one clip (2K1C) model of renin-dependent hypertension. The activation of the MAPK pathways were shown to be crucial in the intracellular signaling leading to cardiac hypertrophy. Therefore, we followed also the cardiac activation of JNK, ERK and the p38 kinase in these animals. Both wild-type and FGF-2 deficient (FGF-2 -/-) mice showed similar elevation of blood pressure in the 2K1C model. Interestingly, 2K1C FGF-2 -/- mice developed markedly reduced hypertrophy as compared to wild-types. Moreover, in 2K1C wild-types, cardiac hypertrophy developed in association with a concomitant stimulation of JNK, ERK and p38. In contrast, JNK activation was strongly decreased in hypertensive mice deficient for FGF-2, while p38 and ERK were less affected. These data suggest that FGF-2 is important in mediating angiotensin II-induced cardiac hypertrophy in renovascular hypertension via autocrine/paracrine mechanisms.

scholarly journals Novel Nuclear Signaling Pathway Mediates Activation of Fibroblast Growth Factor-2 Gene by Type 1 and Type 2 Angiotensin II Receptors

2001 ◽  
Vol 12 (2) ◽  
pp. 449-462 ◽  
Author(s):  
Hu Peng ◽  
John Moffett ◽  
Jason Myers ◽  
Xiaohong Fang ◽  
Ewa K. Stachowiak ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Nuclear Translocation ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Fgf Receptor ◽  
Responsive Element

In bovine adrenal medullary cells synergistically acting type 1 and type 2 angiotensin II (AII) receptors activate the fibroblast growth factor-2 (FGF-2) gene through a unique AII-responsive promoter element. Both the type 1 and type 2 AII receptors and the downstream cyclic adenosine 1′,3′-monophosphate- and protein kinase C-dependent signaling pathways activate the FGF-2 promoter through a novel signal-transducing mechanism. This mechanism, which we have named integrative nuclear FGF receptor-1 signaling, involves the nuclear translocation of FGF receptor-1 and its subsequent transactivation of the AII-responsive element in the FGF-2 promoter.

scholarly journals The Inhibitory Effect of Propylene Glycol Alginate Sodium Sulfate on Fibroblast Growth Factor 2-Mediated Angiogenesis and Invasion in Murine Melanoma B16-F10 Cells In Vitro

Marine Drugs ◽  
2019 ◽  
Vol 17 (5) ◽  
pp. 257 ◽  
Author(s):  
He Ma ◽  
Peiju Qiu ◽  
Huixin Xu ◽  
Ximing Xu ◽  
Meng Xin ◽  
...  
Keyword(s):  
Growth Factor ◽  
Matrix Metalloproteinase ◽  
Fibroblast Growth Factor ◽  
Propylene Glycol ◽  
Sodium Sulfate ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Murine Melanoma ◽  
Melanoma B16 ◽  
Propylene Glycol Alginate

Melanoma is one of the most malignant and aggressive types of cancer worldwide. Fibroblast growth factor 2 (FGF2) is one of the critical regulators of melanoma angiogenesis and metastasis; thus, it might be an effective anti-cancer strategy to explore FGF2-targeting drug candidates from existing drugs. In this study, we evaluate the effect of the marine drug propylene glycol alginate sodium sulfate (PSS) on FGF2-mediated angiogenesis and invasion. The data shows that FGF2 selectively bound to PSS with high affinity. PSS inhibited FGF2-mediated angiogenesis in a rat aortic ring model and suppressed FGF2-mediated invasion, but not the migration of murine melanoma B16-F10 cells. The further mechanism study indicates that PSS decreased the expression of activated matrix metalloproteinase 2 (MMP-2) and matrix metalloproteinase 9 (MMP-9), and also suppressed their activity. In addition, PSS was found to decrease the level of Vimentin in B16-F10 cells, which is known to participate in the epithelial–mesenchymal transition. Notably, PSS did not elicit any changes in cancer cell viability. Based on the results above, we conclude that PSS might be a potential drug to regulate the tumor microenvironment in order to facilitate the recovery of melanoma patients.

Sign in / Sign up

Export Citation Format

Share Document