Fibroblast growth factor-2 interaction with vascular cells and basement membrane under physiological fluid flow and diabetic hyperglycemia

2021 ◽  
Author(s):  
Karl Vernon Reisig
Keyword(s):  
Fluid Flow ◽  
Growth Factor ◽  
Basement Membrane ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 2 ◽  
Vascular Cells ◽  
Fibroblast Growth ◽  
Physiological Fluid

Fibroblast growth factor-2 during postnatal development of the tracheal basement membrane zone

2002 ◽  
Vol 283 (6) ◽  
pp. L1263-L1270 ◽  
Author(s):  
Michael J. Evans ◽  
Michelle V. Fanucchi ◽  
Laura S. Van Winkle ◽  
Gregory L. Baker ◽  
April E. Murphy ◽  
...  
Keyword(s):  
Growth Factor ◽  
Basement Membrane ◽  
Fibroblast Growth Factor ◽  
Structural Changes ◽  
Growth Factor Receptor ◽  
Basement Membrane Zone ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Basal Cells ◽  
Functional Components

Thickening of the basement membrane zone (BMZ) is a characteristic of several airway diseases; however, very little is known about how this process occurs. The purpose of this study was to define development of the BMZ in the trachea of growing rhesus monkeys at 1, 2, 3, and 6 mo of age. We measured immunoreactivity of collagen types I, III, and V to detect structural changes in the developing BMZ. To detect more dynamic, functional components of the epithelial-mesenchymal trophic unit, we evaluated the distribution of perlecan, fibroblast growth factor-2 (FGF-2), and fibroblast growth factor receptor-1 (FGFR-1). One-month-old monkeys had a mean collagen BMZ width of 1.5 ± 0.7 μm that increased to 4.4 ± 0.4 μm in 6-mo-old monkeys. Perlecan was localized in the BMZ of the epithelium at all ages. FGF-2 was strongly expressed in basal cells at 1–3 mo. At 6 mo, FGF-2 was expressed throughout the BMZ and weakly in basal cells. FGFR-1 immunoreactivity was expressed by basal cells and cilia and weakly in the nuclei of columnar cells at all time points. These data indicate that development of the BMZ is a postnatal event in the rhesus monkey that involves FGF-2.

A Computational Model of Fibroblast Growth Factor-2 Binding to Isolated and Intact Cell Surface Receptors: Effects of Fibroblast Growth Factor-2 Concentration, Flow and Delivery Mode

2012 ◽  
Author(s):  
Nisha S. Patel ◽  
Alisa Morss Clyne
Keyword(s):  
Fluid Flow ◽  
Growth Factor ◽  
Computational Model ◽  
Fibroblast Growth Factor ◽  
Binding Kinetics ◽  
Fibroblast Growth Factor 2 ◽  
Delivery Mode ◽  
Fibroblast Growth ◽  
Fibroblast Growth Factor Receptors ◽  
Static Conditions

Fibroblast growth factor-2 (FGF2) plays an important role in both healthy vascular cell functions and pathogenesis in cancer, atherosclerosis and reduced perfusion in diabetes (1–4). FGF2 therapy and targeted drug delivery have great potential in the treatment of such diseases, but have had little clinical success. FGF2 binding kinetics to heparan sulfate proteoglycan (HSPG) and fibroblast growth factor receptors (FGFR) have been largely studied under static conditions (5), however FGF2 binding to endothelial cells occurs physiologically under fluid flow conditions. Understanding complex FGF2 binding kinetics would enable the development of new anti- and pro-angiogenic therapeutics. We developed a computational model of FGF2 binding to FGFR and HSPG with flow to investigate the effect of fluid flow and FGF2 delivery mode on FGF2 binding to isolated or combined binding sites.

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