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. 2014 Jun 13;11(9):870–879. doi: 10.7150/ijms.8758

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© Ivyspring International Publisher. This is an open-access article distributed under the terms of the Creative Commons License (http://creativecommons.org/licenses/by-nc-nd/3.0/). Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited.

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Fig 6 — Ad-Endo-PMSCs inhibited tumor angiogenesis and cell proliferation and induced tumor apoptosis in vivo (1, Control; 2, PMSCs; 3, Ad-Null-PMSCs; 4, Ad-Endo-PMSCs, magnification ×200). A. Immunofluorescence assay of CD31. The Ad-Endo-PMSCs group showed a significant decrease in vessel density compared to the control groups. Vessel density was determined by quantification of the number of the vessels from five high-power fields. Values were expressed as the mean ± SD (*p < 0.05). B. Inhibition of cell proliferation within the tumor estimated using Ki67 immunohistochemical analysis. Tumors of the Ad-Endo-PMSCs group showed a decreased number of Ki67-positive cells compared to the other groups, particularly the NS groups. The proliferation index was determined by counting the number of the Ki67-positive cells from five high-power fields. Values were expressed as the mean ± SD (5 high power fields/slide, *p< 0.05). C. Apoptotic cells from CT26 tumors were detected using the TUNEL assay. The apoptotic index was calculated by dividing the number of TUNEL-positive cells by the total number of cells. Values were expressed as the mean ± SD (five high-power fields/slide,*p< 0.05).