Fig. 2: PlGF123–141-fused IL-1Ra and PDGF-BB strongly bind ECM and are retained in skin tissue. | Communications Biology

Fig. 2: PlGF123–141-fused IL-1Ra and PDGF-BB strongly bind ECM and are retained in skin tissue.

From: Restoration of the healing microenvironment in diabetic wounds with matrix-binding IL-1 receptor antagonist

Fig. 2

a Amino-acid sequences of PlGF fragments fused to glutathione S-transferase (GST). b ELISA plates were coated with ECM proteins and incubated with PlGF fragments. Graphs show signals given when detecting GST. PlGF123–141 is shown in red. n = 4. c PlGF123–141 (in red) was added to the C terminus of IL-1Ra (in pink) or PDGF-BB (in blue) to generate IL-1Ra/PlGF123–141 and PDGF-BB/PlGF123–141. PDGF-BB occurs as a dimer. d Schematic representation of the ECM-mimetic hydrogel and skin endogenous ECM. Fg fibrinogen, Fn fibronectin, Vn vitronectin, TnC tenascin C, HS heparan sulfate. e ECM-mimetic hydrogels were generated with IL-1Ra or PDGF-BB variants and incubated in ten times volume of buffer (with or without plasmin) that was changed every 24 h. The graphs show the cumulative release of IL-1Ra or PDGF-BB variants in buffer. n = 4. f The percentage of IL-1Ra and PDGF-BB variants remaining in skin after intradermal injection was measured at various time points. n = 4 per time point. For (b), (e) and (f), data are means ± SEM. For (b), one-way ANOVA with Bonferroni post hoc test for pair-wise comparisons. For (e) and (f), two-way ANOVA with Bonferroni post hoc test for pair-wise comparisons. *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001.

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