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Results: 4

1.
Figure 4

Figure 4. Microbead perfusion.. From: Targeted In Vivo Extracellular Matrix Formation Promotes Neovascularization in a Rodent Model of Myocardial Infarction.

High magnification (40×) images within the MI region showing the perfusion of 0.2 µm fluorescent microbeads (green) into arterioles that have been stained using anti-α smooth muscle actin (orange) in hearts treated with (a) Ab-FC/HV, (b) Ab-RGD, (c) Ab-HepI, or (d) Ab-HepIII. Scale bar: 15 µm.

Shirley S. Mihardja, et al. PLoS One. 2010;5(4):e10384.
2.
Figure 2

Figure 2. Immunostaining for Ab-HepIII in the infarct region.. From: Targeted In Vivo Extracellular Matrix Formation Promotes Neovascularization in a Rodent Model of Myocardial Infarction.

Hearts from rats sacrificed on 1 day after injection. The rats were injected intravenously with either (a) PBS or (b) the Ab-HepIII 1 day post-MI. The presence of the Ab is indicated by the brown stain. For the sake of clarity, we have outlined the infarct region. At high magnification, we were also able to see fluorescence within the infarct region(c), as indicated by the arrow, of the FITC-labeled peptides (indicated in black).

Shirley S. Mihardja, et al. PLoS One. 2010;5(4):e10384.
3.
Figure 3

Figure 3. Increased neovascularization within the MI region.. From: Targeted In Vivo Extracellular Matrix Formation Promotes Neovascularization in a Rodent Model of Myocardial Infarction.

(a) Capillary staining showed significantly higher capillary density for rats treated with Ab-HepI, Ab-HepIII, or Ab-RGD. † P<0.05 vs. PBS, ‡ P<0.05 vs. Ab-FC/HV. (b) Arteriole staining also showed significantly higher arteriole density for rats treated with Ab-HepI, Ab-HepIII, or Ab-RGD. † P<0.05 vs. PBS, ‡ P<0.05 vs. Ab-FC/HV. (c) Infarct size measurements showed no statistically significant differences between the treatment groups and the PBS treatment group.

Shirley S. Mihardja, et al. PLoS One. 2010;5(4):e10384.
4.
Figure 1

Figure 1. In vitro assays.. From: Targeted In Vivo Extracellular Matrix Formation Promotes Neovascularization in a Rodent Model of Myocardial Infarction.

(a) and (b) Cell adhesion was assessed after 30 minutes of incubation in wells coated with peptides at 20 µg/mL, 50 µg/mL, and 100 µg/mL. The absorbance readings were normalized to either 100 µg/mL FN or 100 µg/mL Col IV, depending on the peptide's source protein, to allow for comparison. * P<0.05. (c) and (d) Cell proliferation was also assessed with peptides at 20 µg/mL, 50 µg/mL, and 100 µg/mL at Day 1 (white), Day 2 (gray), and Day 3 (black). The absorbance readings again were normalized to either 100 µg/mL FN or 100 µg/mL Col IV, depending on the peptide's source protein. (e) and (f) Haptotactic migration at various peptide or protein concentrations. The area cell densities have been normalized to allow for comparison. (g) Western blot analysis showed phosphorylation of Erk1/2 in cells grown on HepI, HepIII, Col IV, RGD, FC/HV, and FN (Wells 1–6, respectively). No phosphorylated Erk1/2 band was seen for cells grown on PBS-treated dishes (Well 7). Total Erk1/2 was present in the cells grown under all the conditions. β-tubulin was used as an internal control.

Shirley S. Mihardja, et al. PLoS One. 2010;5(4):e10384.

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