BMP-2 Genome-Edited Human MSCs Protect against Cartilage Degeneration via Suppression of IL-34 in Collagen-Induced Arthritis.
Dong Sik ChaeSeong-Ho HanMin-Kyung LeeSung-Whan KimPublished in: International journal of molecular sciences (2023)
Even though the regenerative potential of mesenchymal stem cells (MSCs) has been extensively studied, there is a debate regarding their minimal therapeutic properties. Bone morphogenetic proteins (BMP) are involved in cartilage metabolism, chondrogenesis, and bone healing. In this study, we aimed to analyze the role of genome-edited BMP-2 overexpressing amniotic mesenchymal stem cells (AMMs) in a mouse model of collagen-induced arthritis (CIA). The BMP-2 gene was synthesized and inserted into AMMs using transcription activator-like effector nucleases (TALENs), and BMP-2-overexpressing AMMs (AMM/B) were sorted and characterized using quantitative reverse transcription polymerase chain reaction (qRT-PCR). The co-culture of AMM/B with tumor necrosis factor (TNF)-α-treated synovial fibroblasts significantly decreased the levels of interleukin (IL)-34. The therapeutic properties of AMM/B were evaluated using the CIA mouse model. The injection of AMM/B attenuated CIA progression and inhibited T helper (Th)17 cell activation in CIA mice. In addition, the AMM/B injection increased proteoglycan expression in cartilage and decreased the infiltration of inflammatory cells and factors, including IL-1β, TNF-α, cyclooxygenase (COX)-2, and Nuclear factor kappa B (NF-kB) in the joint tissues. Therefore, editing the BMP-2 genome in MSCs might be an alternative strategy to enhance their therapeutic potential for treating cartilage degeneration in arthritic joints.
Keyphrases
- mesenchymal stem cells
- nuclear factor
- umbilical cord
- rheumatoid arthritis
- crispr cas
- mouse model
- cell therapy
- toll like receptor
- bone marrow
- extracellular matrix
- genome editing
- genome wide
- high glucose
- bone regeneration
- transcription factor
- induced apoptosis
- oxidative stress
- endothelial cells
- diabetic rats
- dendritic cells
- regulatory t cells
- gene expression
- signaling pathway
- stem cells
- bone mineral density
- poor prognosis
- insulin resistance
- wound healing
- nitric oxide
- type diabetes
- ultrasound guided
- high resolution
- single cell
- drug induced
- copy number
- bone loss
- adipose tissue
- inflammatory response
- dna methylation
- climate change
- lps induced
- cell proliferation
- body composition
- cell cycle arrest