Analyses of collagen scaffold structure in CT26 and LM3 carcinomas grown in WT and integrin β₃-deficient mice.

<p><b>A</b>) Representative scanning electron micrographs at ×10,000 magnification revealed thicker, fused collagen fibers in both CT26 tumors (n = 5 per genotype) and LM3 tumors (n = 3 per genotype) grown in integrin β₃-deficient mice (bars = 5 µm). <b>B</b>) Ultrastructural analysis of CT26 tumors (n = 5 per genotype) and LM3 tumors (n = 3 per genotype). Representative transmission electron micrographs on collagen fibril morphology demonstrated a heterogeneous fibril diameter distribution in CT26 tumors and LM3 tumors (at ×15,500 and ×11,500 magnification, respectively) grown in integrin β₃-deficient compared to WT mice. Some of the fibrils were laterally fused (white arrowheads) in tumors grown in β₃-deficient mice (bars = 500 nm). Histogram on collagen fibril distribution in CT26 tumors grown in integrin β₃-deficient (black bars; n = 2159) and WT mice (white bars; n = 2043) and in LM3 tumors from integrin β₃-deficient (black bars; n = 1286) and WT mice (white bars; n = 791), showing a clear shift toward thicker fibrils in both tumor types grown in integrin β₃-deficient mice. <b>C</b>) Representative micrographs on tail dermis collagen fibrils from WT and integrin β₃-deficient mice showed similar fibril distribution between the two genotypes (n = 2; bar = 500 nm). No significant difference could be observed in collagen fibril distribution from tail dermis derived from β₃-deficient (black bars; n = 1157) or WT mice (white bars; n = 1715). To analyze fibril distribution, each data point (diameter for each fibril) was tabulated in GraphPad using the Frequency distribution analysis tool.