Date Available
8-11-2017
Year of Publication
2017
Degree Name
Master of Science in Biomedical Engineering
Document Type
Master's Thesis
College
Engineering
Department/School/Program
Biomedical Engineering
First Advisor
Dr. Hainsworth Y. Shin
Abstract
Fluid pressures regulate endothelial cell (EC) tubulogenic activity involving fibroblast growth factor 2 (FGF-2) and its receptor, FGF receptor 2 (FGFR2). Our lab has recently shown that sustained 20 mmHg hydrostatic pressure (HP) upregulates EC sprout formation in a FGF2-dependent fashion. This upregulation of sprout formation may be due to enhanced FGF-2 / FGFR2 interactions in the presence of 20 mmHg HP. We hypothesize that exposure of ECs to 20 mmHg sustained HP enhances FGF-2 binding kinetics. We used a custom hydrostatic pressure system, immunofluorescence, and FACS to quantify FGF-2 binding by ECs in the absence or presence of a range of HPs for 30 minutes. Relative to cells maintained under control pressure, ECs exposed to 20, but neither 5 nor 40 mmHg, displayed a significant increase in binding affinity to FGF-2. EC binding of VEGF-A, another angiogenic growth factor, was unaffected by similar pressure stimuli. Additional studies showed that pressure-selective FGF-2 binding was independent of FGFR2 surface expression. These results implicate the FGF-2 axis in the pressure-sensitive, magnitude-dependent angiogenic processes which we have previously described. The present study provides novel insight regarding the involvement of FGF-2 signaling and interstitial pressure changes in various microvascular physiological and pathobiological processes.
Digital Object Identifier (DOI)
https://doi.org/10.13023/ETD.2017.395
Recommended Citation
McKenty, Taylor R., "QUANTIFYING THE EFFECTS OF HYDROSTATIC PRESSURE ON FIBROBLAST GROWTH FACTOR-2 BINDING BY THE HUMAN ENDOTHELIUM" (2017). Theses and Dissertations--Biomedical Engineering. 47.
https://uknowledge.uky.edu/cbme_etds/47
