05) ( Fig. 3E). CD31, a vascular cell-specific cell–cell adhesion molecule, has been identified to play an important part in the process of angiogenesis. We stained CD31 to investigate

the angiogenesis ability in different transplant sites (Fig. 3C). The quantities of CD31+ blood vessels in various syngeneic grafts were significantly different (P = 0.0002): intra-omental syngeneic grafts had more CD31+ blood vessels than subcutaneous syngeneic grafts (P < 0.05), which had more than orthotopic syngeneic grafts (P < 0.05). The quantities of CD31+ blood vessels in various allografts were also significantly different (P = 0.0093): the quantity of CD31+ blood vessels in EX 527 cost orthotopic allografts was more than heterotopic allografts (P < 0.05), while the quantities were not significantly different between two heterotopic allografts (P > 0.05). Compared with the corresponding syngeneic grafts,

all of the allografts had revascularization at lower level (P < 0.05) ( Fig. 4A). Myofibroblasts with capacity of collagen synthesis are involved in Sirolimus in vivo tissue remodeling. We used α-SMA as a marker for myofibroblasts to determine the fibrosis degrees in transplanted trachea (Fig. 3D). In syngeneic grafts, myofibroproliferation was nearly undetectable during the observation time, whereas allografts had more proliferation of myofibroblasts in lamina propria of transplanted trachea (P < 0.05). The percentages of α-SMA positive area were not significantly different in syngeneic

grafts (P = 0.5278). The percentages were significantly Tangeritin different in allografts (P = 0.0030): The percentages of α-SMA+ area in two different heterotopic allografts were similar (P > 0.05), but significantly higher than orthotopic allografts (P < 0.05) ( Fig. 4B). The optimal tool to study OB pathogenesis, no doubt, is human lung transplantation. However, drawbacks such as sparse OB samples, and difficulties of sampling at various times, in addition to complications after sampling like infections, hamper human lung transplantation to act as a “model”. There is therefore a critical need for some animal models that could elucidate the pathogenesis of OB. Of the different tracheal transplantation models employed in this study, each has obvious advantages and drawbacks [15], and previous investigators have not yet come to a consistent conclusion on which of the transplantation models is more qualified as a model for studying OB. Since evidence is mounting that epithelial damage [16] and [17], immune-mediated tissue injury [18], angiogenesis [19] and [20] and fibroproliferative remodeling [21] may be involved in the development of OB, we compared transplantation models in terms of these hotspot issues in this study. In addition, we combined transplantation models to decrease the consumption of the animals as well as improve individual error and the experimental efficiency.