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To develop a naturally derived tendon tissue engineering scaffold with the preservation of the native ultrastructure, tensile strength, and biochemical composition of the tendon extracellular matrix (ECM), decellularized tendon slices (DTSs) were prepared using repetitive freeze/thaw of the intact Achilles tendons, frozen section, and nuclease treatment. The DTSs were characterized in the native ultrastructure, mechanical properties, biochemical composition, and cytocompatibility. Histological examination and DNA quantification analysis confirmed that cells were completely removed from tendon tissue by repetitive freeze/thaw in combination with nuclease treatment 12 h. The intrinsic ultrastructure of tendon tissue was well preserved based on scanning electron microscopy examination. The tensile strength of the DTSs was retained 85.62% of native tendon slice. More than 93% of proteoglycans (fibromodulin, biglycan) and growth factors (TGF-β1, IGF-1, VEGF, and CTGF) inherent in tendon ECM were preserved in the DTSs according to ELISA analysis. Furthermore, the DTSs facilitated attachment and repopulation of NIH-3T3 fibroblasts in vitro. Overall, the DTSs are sheet scaffolds with a combination of elemental mechanical strength and tendon ECM bioactive factors that may have many potential applications in tendon tissue engineering.

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Mesenchymal stem cells (MSCs) are the most promising seed cells for cell therapy and tissue engineering, which can be isolated from various sources of human adult tissues such as bone marrow and adipose tissue. However, cells from these tissues must be obtained through invasive procedures and sometimes the individual difference is hard to control. Hence, the search continues for an ethically conducive, easily accessible and controllable source of stem cells. We herein report the isolation of a population of stem cells from the human placental decidua basalis (termed as PDB-MSCs), a maternal portion of placenta. PDB-MSCs were further shown to express markers common to MSCs and positive for SSEA-1, SSEA-3, SSEA-4, TRA-1-60, TRA-1-81 and Oct-4. In order to facilitate the further utility in ischemic diseases, we tested the apoptosis of PDB-MSCs in hypoxia and serum deprivation, two components of ischemia in vivo. Taken together, our findings indicate that PDB-MSCs are resistant to hypoxia and serum deprivation, which may relate to Bcl-2.

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