Publications by authors named "Sehee Cho"

Chondrocyte hypertrophy has been implicated in endochondral ossification and osteoarthritis (OA). In OA, hypertrophic chondrocytes contribute to the destruction and focal calcification of the joint cartilage. Although studies in this field have remarkably developed the modulation of joint inflammation using gene therapy and regeneration of damaged articular cartilage using cell therapy, studies that can modulate or prevent hypertrophic changes in articular chondrocytes are still lacking.

View Article and Find Full Text PDF
Article Synopsis
  • There’s a protein called PUM1 that helps keep special cells called mesenchymal stem cells (MSCs) from aging too quickly and becoming unhealthy.
  • PUM1 does this by working with another protein called TLR4, which influences how MSCs behave, especially when there's inflammation.
  • Researchers found that increasing PUM1 helps protect these cells and even shows promise for treating osteoarthritis, a disease that affects joints.
View Article and Find Full Text PDF

Despite several studies on the effect of adeno-associated virus (AAV)-based therapeutics on osteoarthritis (OA), information on the transduction efficiency and applicable profiles of different AAV serotypes to chondrocytes in hard cartilage tissue is still limited. Moreover, the recent discovery of additional AAV serotypes makes it necessary to screen for more suitable AAV serotypes for specific tissues. Here, we compared the transduction efficiencies of 14 conventional AAV serotypes in human chondrocytes, mouse OA models, and human cartilage explants obtained from OA patients.

View Article and Find Full Text PDF

Purpose: Our previous work demonstrated that miRNA-495 targets SOX9 to inhibit chondrogenesis of mesenchymal stem cells. In this study, we aimed to investigate whether miRNA-495-mediated SOX9 regulation could be a novel therapeutic target for osteoarthritis (OA) using an in vitro cell culture model.

Materials And Methods: An in vitro model mimicking the OA environment was established using TC28a2 normal human chondrocyte cells.

View Article and Find Full Text PDF