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Figure 3 | BMC Systems Biology

Figure 3

From: Formation of VEGF isoform-specific spatial distributions governing angiogenesis: computational analysis

Figure 3

Steady-state distribution of VEGF is not dependent upon interstitial HSPGs. Using the model, we calculated the steady-state distribution of VEGF165, in the presence (A) and absence (B) of interstitial HSPGs, assuming no interstitial proteases, and no other differences between the two systems. The VEGF distribution was initialized so as to have a mean soluble VEGF concentration of ~1 pM and a fractional gradient of ~5%/40 μm at the leading edge of the sprout (z = 0); HSPG binding and receptor-mediated internalized were calculated. Conditions of the model are defined in Table 4: HSPG = 750 nM, VEGFR1 = VEGFR2 = 104/cell, NRP1 = 3*104/cell; secretion and clearance of the soluble fraction occurred at q = 5.27·10-5 molec/μm2·sec and kclear = 0.0399 μm/sec. Traces of steepest descent arising from r = 0, 6, 20, and 38 μm and z = 80 μm are overlaid to demonstrate the effect of internalization on the curvature of the VEGF distribution around the sprout. We also measured VEGFR1, VEGFR2, and NRP1 receptor occupancies, absolute and fractional gradients, and the sensitivity of relative gradient detection are given for each case. The sensitivity is defined as the ratio of the receptor gradient to the ligand gradient.

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