Details

Autor(en) / Beteiligte

• Delgado-Enciso, Ivan
• Paz-Garcia, Juan
• Rodriguez-Hernandez, Alejandrina
• Madrigal-Perez, Violeta M
• Cabrera-Licona, Ariana
• Garcia-Rivera, Alejandro
• Soriano-Hernandez, Alejandro D
• Cortes-Bazan, Jose L
• Galvan-Salazar, Hector R
• Valtierra-Alvarez, Jose
• Guzman-Esquivel, Jose
• Rodriguez-Sanchez, Iram P
• Martinez-Fierro, Margarita L
• Paz-Michel, Brenda

Titel

A promising novel formulation for articular cartilage regeneration: Preclinical evaluation of a treatment that produces SOX9 overexpression in human synovial fluid cells

Ist Teil von

• Molecular medicine reports, 2018-03, Vol.17 (3), p.3503-3510

Ort / Verlag

Greece: Spandidos Publications

Erscheinungsjahr

2018

Quelle

EZB Electronic Journals Library

Beschreibungen/Notizen

• Osteoarthritis (OA) is a chronic disorder of synovial joints, in which there is progressive softening and disintegration of the articular cartilage. OA is the most common form of arthritis, and is the primary cause of disability and impaired quality of life in the elderly. Despite considerable medical necessity, no treatment has yet been proven to act as a disease‑modifying agent that may halt or reverse the structural progression of OA. The replacement of the joint with a prosthesis appears to be the best option in the advanced stages of the disease. A formulation (BIOF2) for cartilage regeneration has been recently developed. The present study evaluated the effects of BIOF2 on gene expression in human cell cultures, followed by efficacy trials in three OA animal models. Human synovial fluid cells that were exposed to the formulation exhibited increased transcription factor SOX‑9 (SOX9; chondrogenic factor) expression, and decreased mimecan (mineralization inducer) and macrophage‑stimulating protein receptor (osteoclastogenic factor) expression. The intra‑articular application of BIOF2 in the animal models significantly increased cartilage thickness from 12 to 31% at 28 days, compared with articular cartilage treated with saline solution. The articular area and number of chondrocytes additionally increased significantly, maintaining an unaltered chondrocyte/mm2 proportion. Evaluation of the histological architecture additionally displayed a decrease in the grade of articular damage in the groups treated with BIOF2. In conclusion, BIOF2 has proven to be effective for treating OA in animal models, most likely due to SOX9 overexpression in articular cells.