We found that ASMSCs possessed an abnormal osteogenic capacity, which may contribute to the pathogenesis of AS.
In our study, we found that ASMSCs were more susceptible to TNF-[alpha]-induced apoptosis compared to HDMSCs, as evidenced by an increased apoptosis rate and the higher expression of cleaved caspase-3 protein.
In patients with AS, increased apoptosis of ASMSCs may result in decreases in cell numbers and immunosuppressive potential, eventually contributing to autoimmune disorders.
In our study, we observed a significant increased expression of TRAIL-R2 in ASMSCs after treatment with TNF-[alpha]/CHX.
In this study, we demonstrated that TRAIL-R2 upregulation resulted in enhanced apoptosis of ASMSCs. Increased apoptosis of ASMSCs may decrease the immunosuppressive potential of these cells and potentially contributing to AS pathogenesis.
Caption: FIGURE 1: HDMSCs and ASMSCs shared the same morphology, phenotype, and proliferation capacity.
Caption: FIGURE 2: ASMSCs were more susceptible to TNF-[alpha]/CHX-induced apoptosis compared to HDMSCs.
Caption: FIGURE 3: ASMSCs had increased protein expression of cleaved caspase-3, TRAIL-R2, and FADD and increased gene expression of TRAILR2 and FADD during apoptosis.
(a) qRT-PCR was performed to compare the gene expressions of total caspase-8, total cytochrome C, Fas, and TNFR1 between HDMSCs (n = 28) and ASMSCs (n = 22).