Nanomaterials and Nanotechnology

Biography

Biography: Sang Jun Kim

Abstract

Introduction: Identification of the tendon derived stem cells (TDSCs) suggests a new paradigm to develop a new treatment of tendon healing. Provision of adequate environment to differentiate these stem cells into normal tenocytes becomes an important issue. However, there has been no knowledge about the control of the TDSCs to repair the damaged tendon tissues in tendinopathy. The purpose of this study is to investigate how nano-topographic signals control the TDSCs extracted from diverse tendon status. Methods: TDSCs were primarily cultured and isolated from the tendon tissues of 5-week old normal Sprague-Dawley (SD) rats (n=2), 15-week old normal SD rats (n=2), and a 38-week old normal SD rat (n=1) and from the tendon tissues of 5-week old SD rats with tendinopathy (n=2) and 15-week old SD rats with tendinopathy (n=2). They were cultured on the diverse nano-topographic matrices; (1) 19.8 MPa surface stiffness with 800 nm width nano-groove, (2) 2.4 GPa with 800 nm, and (3) 2.4 GPa without groove (flat surface) until reaching confluence of 80%. If TDSCs did not reach the confluence, β-galactosidase staining was done to check the senescence. Doubling time was calculated for the proliferative capacity in each condition. Differentiation capacity was evaluated under the chondrogenic, adipogenic, and osteogenic condition. Major components of tendon including collagen type I (Col1), collagen type III (Col3), and decorin were expressed for the reparative capacity by the immunofluorescent staining and qRT-PCR. Results: Proliferative capacities were not significantly different according to the age or pathological condition except TDSCs from 38-week old rat which were not proliferated and underwent the senescent process. Osteogenic differentiation was strong in 5-week old tendinopathy and adipogenic differentiation was strong in 15-week old tendinopathy. In TDSCs from 5-week and 15-week old normal rats, protein expression of Col1 and the ratio of Col1/Col3 in 19.8 MPa plate with 800 nm nano-topographic grooves were significantly higher than other plates. This difference according to the nano-topographic signals and surface stiffness was not found in TDSCs from 5-week old tendinopathy and 15-week old tendinopathy. This was consistent with the gene expression in qRT-PCR analysis. Conclusion: TDSCs extracted from normal tendon show the best reparative capacity in a specific condition (19.8 MPa with 800 nm nano-topographic grooves), which is similar to the normal in-vivo status. However, this preference is disturbed in tendinopathy, which results in aberrant differentiation of TDSCs. To restore the tendon function properly in tendinopathy, we must consider these characteristics of TDSCs and find the optimal conditions to induce the Col1 expression and to prevent the aberrant differentiation.