FIBROBLAST GROWTH FACTOR (FGF-2) PREVENTS HUMAN CARDIAC FIBROBLAST-MEDIATED EXTRACELLULAR MATRIX REMODELING

2014 ◽  
Vol 30 (10) ◽  
pp. S153 ◽  
Author(s):  
D.A. Svystonyuk ◽  
J.M. Ngu ◽  
H.E. Mewhort ◽  
D.G. Guzzardi ◽  
B.D. Lipon ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Cardiac Fibroblast ◽  
Extracellular Matrix Remodeling ◽  
Matrix Remodeling ◽  
Fibroblast Growth

scholarly journals ColXV Aggravates Adipocyte Apoptosis by Facilitating Abnormal Extracellular Matrix Remodeling in Mice

2020 ◽  
Vol 21 (3) ◽  
pp. 959
Author(s):  
Xia ◽  
Shen ◽  
Cai ◽  
Pan ◽  
Sun
Keyword(s):  
Extracellular Matrix ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Growth Factor Receptor ◽  
Collagen Matrix ◽  
Basement Membranes ◽  
Matrix Remodeling ◽  
Fibroblast Growth ◽  
Adipose Tissues ◽  
Ecm Remodeling

The extracellular matrix (ECM) is a highly dynamic structural network and plays an essential role in cell behavior and regulation during metabolic homeostasis and obesity progression. Abnormal ECM remodeling impairs adipocyte plasticity required for diverse cellular functions. Collagen XV (ColXV) is a proteoglycan localized to the outermost layer of basement membranes (BMs) and forms a bridge between the BMs and the fibrillar collagen matrix. Nevertheless, how ColXV affects ECM composition and the reason for subsequent adipocyte apoptosis is still unclear. This report found, through RNA-seq data, that ColXV is linked to cell growth and ECM remodeling. Findings show that, in response to excessive expression of extracellular ColXV, the AMPK/mTORC1 pathway is strongly activated and triggers a cascade of mitochondrial apoptosis. This is the first study to make use of ECM three-dimensional reconstruction, based on decellularization in the adipose tissues and the study reveals that ColXV is an activation factor that alters ECM remodeling in adipose tissues. It was also demonstrated that the fibroblast growth factor 2 (FGF2)/fibroblast growth factor receptor 1 (FGFR1) axis involved in ECM remodeling is suppressed by ColXV due to reduction of FGF2 translocation to FGFR1. Furthermore, ColXV induced remodeling of ECM preceding apoptosis and continued to induce apoptosis in adipocytes. Collectively, our findings establish ColXV as a basement membrane collagen with homology to ColXVIII, indicating that it is one of the positive regulators for inducing ECM remodeling and further promoting adipocyte apoptosis.

scholarly journals Heparin and heparan sulfate increase the radius of diffusion and action of basic fibroblast growth factor.

1990 ◽  
Vol 111 (4) ◽  
pp. 1651-1659 ◽  
Author(s):  
R Flaumenhaft ◽  
D Moscatelli ◽  
D B Rifkin
Keyword(s):  
Extracellular Matrix ◽  
Growth Factor ◽  
Heparan Sulfate ◽  
Fibroblast Growth Factor ◽  
Morphological Changes ◽  
Fibroblast Growth ◽  
Soluble Phase ◽  
Heparan Sulfates ◽  
Sulfate Complexes

The radius of diffusion of basic FGF (bFGF) in the presence and in the absence of the glycosaminoglycans heparin and heparan sulfate was measured. Iodinated 125I-bFGF diffuses further in agarose, fibrin, and on a monolayer of bovine aortic endothelial (BAE) cells in the presence of heparin than in its absence. Heparan sulfates affected the diffusion of 125I-bFGF in a manner similar to, though less pronounced than, heparin. When applied at the center of a monolayer of BAE cells, bFGF plus heparin stimulated morphological changes at a 10-fold greater radius than bFGF alone. These results suggest that bFGF-heparin and/or heparan sulfate complexes may be more effective than bFGF alone in stimulating cells located away from the bFGF source because the bFGF-glycosaminoglycan complex partitions into the soluble phase rather than binding to insoluble glycosaminoglycans in the extracellular matrix. Thus, the complex of bFGF and glycosaminoglycan may represent one of the active forms of bFGF in vivo.

Importance of size and sulfation of heparin in release of basic fibroblast growth factor from the vascular endothelium and extracellular matrix

Biochemistry ◽  
1992 ◽  
Vol 31 (7) ◽  
pp. 2080-2088 ◽  
Author(s):  
Rivka Ishai-Michaeli ◽  
Carl M. Svahn ◽  
Michael Weber ◽  
Tova Chajek-Shaul ◽  
Gil Korner ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Vascular Endothelium ◽  
Fibroblast Growth

scholarly journals The Morphopathogenetic Aspects of Intraabdominal Adhesions in Children under One Year of Age

Medicina ◽  
2019 ◽  
Vol 55 (9) ◽  
pp. 556
Author(s):  
Anna Junga ◽  
Māra Pilmane ◽  
Zane Ābola ◽  
Olafs Volrāts
Keyword(s):  
Extracellular Matrix ◽  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Transforming Growth Factor ◽  
Interleukin 4 ◽  
Relative Distribution ◽  
Fibroblast Growth ◽  
Pgp 9.5 ◽  
Intraabdominal Adhesions ◽  
One Year

Background and Objectives: The morphopathogenesis of adhesions is a complex process, characterized by the accumulation of an extracellular matrix, inflammation and hypoxia. The regulatory role between morphopathogenic factors in adhesions has not yet been defined. The aim was to investigate the appearance of transforming growth factor beta (TGFβ), hepatocyte growth factor (HGF), basic fibroblast growth factor (FGF-2), fibroblast growth factor receptor 1 (FGFR1), vascular endothelial growth factor (VEGF), protein gene product 9.5 (PGP 9.5), chromogranin A (CgA), interleukin-1 alpha (IL-1α), interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-7 (IL-7), interleukin-8 (IL-8), interleukin-10 (IL-10), tumor necrosis factor alpha (TNFα), human beta defensine-2 (HBD-2), matrix metaloproteinase-2 (MMP-2) and matrix metaloproteinase-2 tissue inhibitor (TIMP-2) in intraabdominal adhesions. Materials and Methods: The study material was obtained from 49 patients under one year of age with total or partial bowel obstruction. All factors were detected using immunohistochemistry methods and their relative distribution was evaluated by means of the semiquantitative counting method. Results: Intraabdominal adhesions are characterized by increased TGFβ, FGFR1, VEGF and decreased FGF-2, HGF, PGP 9.5, IL-1, IL-4, IL-8, TIMP-2 findings. The most significant changes observed were the remodulation of the extracellular matrix, promotion of neoangiogenesis and the maintenance of a prolonged inflammation. Conclusions: The increase in TGFβ, relative to the decrease of HGF, as well as the disbalance between MMP-2 and TIMP-2 proves an increased fibrosis in intraabdominal adhesions. Less detected FGF-2 and more prominent FGR1 findings points out a compensatory receptor stimulation in response to the lacking same factor. The decrease in PGP 9.5 and the increase in VEGF-positive macrophages indicate hypoxic injury and proves the stimulation of neoangiogenesis. An unpronounced IL-1 and marked IL-10 finding indicate the local tissue protection reaction, the decrease in IL-4 could be the direct cause of giant cells, but the decrease of IL-8 could confirm a delayed chemotaxis of inflammatory cells.

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