Human umbilical cord derived mesenchymal stem cells induce tissue repair and regeneration in collagen-induced arthritis in rats

Mehak Vohra,Aman Sharma,Rashmi Bagga,Sunil K Arora

doi:10.18053/jctres.06.202006.003

Abstract

The current study highlights the potential use of MSCs as a cell-based therapeutic option for the treatment of inflammatory RA.

Highlights

Rheumatoid arthritis (RA) is a chronic inflammatory disease that primarily affects the joints, causing articular destruction, associated pain, stiffness, and synovitis [1,2]
We found downregulation of factors related to bone destruction such as RANK, receptor activator of nuclear factor-kappa B ligand (RANKL), TRAP, Cathepsin K, MMP3, MMP9, and NFATc1 after treatment with UC-mesenchymal stem/stromal cells (MSCs), suggesting this to be a primary mechanism underlying the reduction of the bone and cartilage damage in the umbilical cord-derived MSCs (UC-MSCs)-treated collagen-induced arthritis (CIA) rats
Our findings support the therapeutic potential of UC-MSCs for autoimmune chronic inflammatory diseases such as rheumatoid arthritis (RA) through allotransplantation

Summary

Introduction

Rheumatoid arthritis (RA) is a chronic inflammatory disease that primarily affects the joints, causing articular destruction, associated pain, stiffness, and synovitis [1,2]. In addition to causing a perturbation of both the innate and adaptive immune responses [3,4], RA has been associated with the presence of circulating autoantibodies against self-proteins and rheumatoid factor [5,6]. Current anti-rheumatic therapies primarily target suppression of inflammatory cascade with limited or no success in controlling progression of bone and cartilage destruction [7]. The inflammation-induced bone loss is mediated mainly by increased osteoclast formation and function. Osteoclasts are formed by the fusion of myeloid precursors of monocyte/macrophage lineage in the presence of receptor activator of nuclear factor-kappa B ligand (RANKL) and macrophage-colony-stimulating factor [8]. The pro-inflammatory milieu of the arthritis synovium leads to Distributed under creative commons license 4.0

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