Fig 1: Evaluation of the potential of hMPB as autologous grafts in rAA replacement model.(A) Subcutaneously prepared hPBs were used as autologous abdominal artery replacements in rats. (B) CDU images of hMPB-V1m and hMPB-V3m and (C) corresponding measurement of luminal diameter. (D) Quantification of in vivo compliance of implanted hMPB and rAA. (E) Lumen and enface views of hMPB-V1m and hMPB-V3m. (F) H&E images of hMPB-V1m, hMPB-V3m, and rAA cross sections; quantification of hMPB neointima thickness shown alongside. Black dashed lines represent PS wall boundary (hMPB, hMPB-V1m, and hMPB-V3m) or boundary between tunicae media and adventitia layers (rAA). (G) EC coverage was visualized and calculated on the basis of anti-eNOS IF staining of hMPB longitudinal sections before and after VI. (H) EC coverage of lumen surfaces of hMPB-V1m and hMPB-V3m observed by SEM. (I) Co-stained cross sections show the distribution of ECs (eNOS, red) and SMCs (MYH, green) in hMPB-V1m, hMPB-V3m, and rAA. White dashed lines represent PS wall boundary (hMPB, hMPB-V1m, and hMPB-V3m) or the boundary between tunicae media and adventitia layers (rAA). (J) MYH+ SMC layer thickness calculated from eNOS/MYH co-staining. (K) Representative curves of physiological functions of hMPB, hMPB-V3m, and rAA in response to vasodilators and vasoconstrictors. (L) Quantification of constriction in response to KCl and AD; (M) Quantification of relaxation in response to ACh and SNP. Samples were preconstricted with AD, and then responses to vasodilators were assessed. Data are representative of n = 5 rats. Unpaired Student’s t test (D and G) and one-way ANOVA followed by Tukey’s test (C, F, J, L, and M) were performed. *P < 0.05, **P < 0.01, ***P < 0.001. NS, not significant.