Background: Breast reconstruction with fat grafting has an unstable retention rate due to insufficient revascularization. Tissue Engineering Chamber (TEC) model can promote tissue regeneration in the chamber by introducing ligated vessels around the tissue. We introduced ligated vessels with free fat graft to investigate the retention rate and revascularization of grafted fat that in TEC model. Methods: SD rats (n=24) was divided into 3 groups randomly. Group A: Standard TEC model was constructed; Group B: the epigastric vessel bundles were dissected from the fat flap and ligated, fat flap was cut into granules and planted into the chamber; Group C: Free fat was planted in the chamber. At week 6, samples in the chamber were harvested. Results: Significant volume increase was observed in group A and B, while the volume decreased in group C (P<0.05). Regeneration morphology could be found according to the histological observation in A and B. Micro CT results showed the ligated vessels into grafted fat sprouting robustly, coordinated with volume changes. Conclusion: Fat grafts in TEC model could not only survive but also regenerate. The combination of fat graft and TEC could fabricate a vascularized fat flap, which was a promising method in breast reconstruction.

Adipose flap expansion using a tissue engineering chamber (TEC) presents a promising candidate for soft tissue regeneration by activating in situ adipose tissue regeneration. However, foreign body reaction (FBR) and capsular contracture caused by a silicone chamber limit large tissue reconstruction. Here, a hydrophilic and biodegradable film made of poly­(ethylene glycol) diacrylate (PEG-da) with methacrylated gelatin (gelatin-MA) was presented between the host tissue and silicone chamber to tune the local wound and to prevent initiation of FBR. After a 60 day investigation, 6.1-fold-regenerated fat tissue was obtained from the PEG–gelatin group, whereas only 3-fold tissue was harvested from a silicone group. Histological staining demonstrated that the structure of the neo-formed adipose tissue in both groups was similar to mature adipose tissue. Noticeably, a more distinct and denser fibrous capsule was observed in the silicone group compared to the PEG–gelatin group. Immunohistochemistry of CD206 and TGF-β expression indicated less M2 macrophage infiltration and a minor inflammation reaction with PEG–gelatin assistance. Less collagen deposition and myofibroblast activation in the PEG–gelatin group were demonstrated via α-SMA and type I collagen staining. All these demonstrated that a biocompatible membrane supplement can attenuate capsule formation and contracture leading to a larger tissue regeneration through the TEC technique, which could lead to new perspectives to the relationship between materials-mattered FBR and tissue regeneration.

Background The role of the transforming growth factor (TGF)-β1/CXC chemokine receptor (CXCR) 7 signaling axis in angiogenesis mediated by endothelial progenitor cells (EPCs) in diabetes mellitus (DM) remains unclear. Methods An in vivo wound healing model was established in mice, which were treated with phosphate-buffered saline (PBS) or TGF-β1. Wound closure rate was measured to evaluate wound healing. Histological analysis and immunofluorescent staining were performed to investigate angiogenesis and the number of EPCs in vivo. EPCs were isolated from bone marrow via gradient centrifugation. An angiogenic medium was used to induce endothelial cells (ECs) from EPCs. Flow cytometry was used to identify EPCs and ECs. Lv-shCXCR7 was used to determine the role of CXCR7 in EPCs in vitro. EPC proliferation was measured via 5-ethynyl-2′-deoxyuridine staining. Scratch and transwell assays were performed to assess EPC migration. Results Remaining wound area from day 7 to 14 in the DM + TGF-β1 group was significantly lower than that in the DM + PBS group but higher than that in the PBS group. On day 14, the number of microvessels in wounds was significantly higher for TGF-β1-treated mice than for mice not treated with TGF-β1. The number of EPCs in the DM + TGF-β1 group was significantly higher than that in the DM + PBS group. The high-glucose environment significantly impaired the proliferation, migration, and tube-forming ability of EPCs; however, TGF-β1 partially restored the proliferation and tube-forming ability of EPCs (p < 0.05). Additionally, shCXCR7 lentiviral transfection resulted in a significant reduction in the proliferation and tube-forming ability of EPCs; however, it had no significant effect on EPC migration. Furthermore, the high-glucose environment caused a decrease in the mRNA and protein expression of CXCR7 in EPCs; however, this was partially reversed by TGF-β1 (p < 0.05). Conclusions Our results show for the first time that TGF-β1 partially restores the proliferation and tube-forming ability of EPCs in a high-glucose environment by upregulating CXCR7 expression, increasing the number of blood vessels, and accelerating wound healing. This novel TGF-β1 pathway may play a potentially therapeutic role from bench to bedside.