Plasma vascular endothelial growth factor, soluble VEGF receptor FLT-1, and von Willebrand factor in glaucoma

Transforming growth factor‐β‐regulated gene transcription and protein expression in human GFAP‐negative lamina cribrosa cells

“…Our observation that LC cells are capable of VEGF release in vitro, suggests a possible mechanism for glaucomatous ONH hemorrhage in vivo, a phenomenon, which is associated with significant progression of visual field loss (Ishida et al, 2000). Further support for the potential role of VEGF in POAG comes from a study showing significantly elevated plasma levels of this protein in POAG patients versus normal IOP age matched controls (Lip et al, 2002). To investigate further the transcriptional control of a TGF-b1 responsive gene in our system, we chose the secreted proteoglycan, endothelial cell-specific molecule-1 (ESM-1).…”

Model of competitive binding of vascular endothelial growth factor and placental growth factor to VEGF receptors on endothelial cells

“…PlGF tissue concentrations in normal placentas were Ͻ4 ng/g tissue (ϳ0.5 nM interstitial PlGF); however, choriocarcinoma tissue concentration was 116 ng/g tissue (42). Measured plasma concentrations of VEGF range from 0.5 to 2 pM and PlGF has been measured at 11 pM (14,20,26,32,33), and serum concentrations have been measured in the ranges of 0.5-4 and 1-11 pM, respectively (44,52). At these lower concentrations, we cannot rule out ligand shifting as a part of the synergistic response (see Fig.…”

“…The results of the simulations show that a thin layer of ECM proteins secreted and remaining close to the cell surface did not significantly increase the ligand shifting in this experiment, up to micromolar concentrations of ECM binding sites. Serum levels of sVEGFR1 in the healthy adult were reported to be 28 ng/ml, or 250 pM (32). This concentration of soluble receptor in the medium would cause a maximum change in VEGF-VEGFR2 formation of 8% (see Fig.…”

The Role of Inflammation in the Pathogenesis of Glaucoma

“…Clinical studies have revealed the presence of increased VEGF in POAG and NTG, suggesting that these patients may suffer from an impaired BRB, which in turn causes vascular dysregulation. 43 Moreover, VEGF correlates with ET-1 in glaucoma patients, 26 indicating that vascular dysregulation arises by giving direct access of ET-1 from the endothelial cells in the choroid to the retina and the ciliary body or vice versa. 73,86 Increased ET-1 in the blood may stimulate ETreceptors of the vascular smooth muscle cells, which causes vasoconstriction and decreased ocular blood flow.…”