Correction to: Type I Diabetes Delays Perfusion and Engraftment of 3D Constructs by Impinging on Angiogenesis; Which can be Rescued by Hepatocyte Growth Factor Supplementation

Correction to: Cellular and Molecular Bioengineering https://doi.org/10.1007/s12195-019-00574-3

The values on the Y-axis for Figs. 1a, 2a, and 5a were in ng/L, not in molar. To meet the CAMB journal requirements, we have converted the values to molar and updated the graphs.

Corrected Figs. 1a, 2a, and 5a are shown below.

Figure 1

HGF is secreted by adipose-derived microvessel fragments in 3D constructs and mediates angiogenic sprouting. (a) In vitro analysis of HGF secretion from pre-vascularized engineered constructs. Pre-vascularized engineered constructs were maintained in 20% FBS-DMEM. Media was collected at the indicated time-points and HGF secretion was measured by ELISA (mean ± SEM; one-way ANOVA, Bonferroni correction, p ≤ 0.0001 vs. day 0). (b) Blockage of HGF/c-MET significantly reduces sprouting angiogenesis. Pre-vascularized constructs were maintained in 20% FBS-DMEM containing either anti-HGF antibody (a-HGF), c-MET inhibitor (SU11274), IgG control, or DMSO (vehicle) for 7 days (mean ± SEM; n = 3 one-way ANOVA, Bonferroni correction, anti-HGF p ≤ 0.05, SU11274, p ≤ 0.0001).

Figure 2

HGF is secreted from cultured perivascular cells. (a) Quantification of HGF secretion from smooth muscle cells or pericytes by ELISA (mean ± SEM; two-way ANOVA, Bonferroni correction; p ≤ 0.0001). (b) HGF expression by perivascular cells was confirmed in vitro in the pre-vascularized engineered constructs. Immunofluorescence staining of HGF at day 5 shows that HGF (red) co-localizes with alpha-smooth muscle cell actin (aSMA, perivascular cell marker, green) but not lectin (endothelial cell marker, blue).

Figure 5

Diabetes impairs HGF secretion and decreases angiogenic sprouting in pre-vascularized engineered constructs. (a) In vitro analysis of HGF secretion from microvessel-based engineered constructs under high glucose conditions. Pre-vascularized tissues containing 20,000 microvessel fragments/ml were maintained in culture for 5 days in DMEM containing 10% FBS with either 25 mM d-glucose or 25 mM mannitol (control). HGF secretion was quantified by ELISA of culture supernatants (mean ± SEM; n = 3; two-way ANOVA, Bonferroni correction, *p = 0.3, **p = 0.0003). (b) Culture in high glucose (25 mM d-glucose) media significantly inhibits sprouting as compared to control (25 mM mannitol) and low glucose (5 mM d-glucose). Data were coded to: 0 = no sprouts; 1 = sprouting; 2 = high sprouting (mean ± SEM; n = 3; one-way ANOVA, Bonferroni correction, *p = 0.01 vs. 25 mM d-mannitol or 5 mM d-glucose).