Researchers report that osteoarthritis is caused by the loss of Gremlin 1 (Grem1)-lineage chondrogenic progenitor cells.
By Tarun Sai LomteNov 3 2023Reviewed by Benedette Cuffari, M.Sc. In a recent study published in Nature Communications, researchers report that osteoarthritis is caused by the loss of Gremlin 1 -lineage chondrogenic progenitor cells.
OA often occurs due to injury, aging, or chronic mechanical stress. The loss of articular cartilage , which has a limited capacity to regenerate, is a characteristic of OA. Study findings In the present study, researchers used two mouse models of induced OA, including collagenase VII-induced OA and surgical destabilization of medial meniscus . These mouse models were used to examine Grem1-lineage cells, Lepr mesenchymal stem cells, and aggrecan -marked articular chondrocytes in OA.
The researchers then investigated whether Grem1 CP cells were the resident stem progenitor cells for normal postnatal AC development and maintenance. To this end, Grem1 CP cells were immediately observed in the meniscus and cartilaginous epiphysis after one week, giving rise to around 40% of the AC. In later developmental stages, Grem1-lineage CP cells generated robust osteoblasts in the subchondral bone, populating the entire joint by one month.
Gene expression was analyzed using single-cell ribonucleic acid sequencing data. Fork-head box protein-o 1 expression correlated with Grem1 expression in articular CP cells and was significantly higher in Grem1-lineage cells in the AC than in the GP. Most cells expressing FOXO1 in the adult AC were of the Grem1 lineage, with fewer FOXO1-expressing Grem1 cells in the GP.
The researchers also examined the impact of exogenous fibroblast growth factor 18 on Grem1-lineage AC stem cells, given its role as an agonist of FGF receptor 3 in experimental OA treatment. To this end, tamoxifen-treated adult Grem1-TdT mice received FGF18 for two weeks, which significantly elevated Grem1-lineage articular CP cells and increased AC thickness.
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