Synovial Fluid Derived from Human Knee Osteoarthritis Increases the Viability of Human Adipose-Derived Stem Cells through Upregulation of FOSL1.
Synovial Fluid Derived from Human Knee Osteoarthritis Increases the Viability of Human Adipose-Derived Stem Cells through Upregulation of FOSL1.
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膝关节骨性关节炎（膝OA）是一种不可逆转的疾病，它会导致组成关节的关节软骨的骨畸形和变性，导致慢性疼痛和运动障碍。体外培养的脂肪源性干细胞（ADSCs）注入膝关节腔改善膝关节OA的临床症状；然而，滑膜液（SF）填充关节腔对注射ADSCs的影响尚不清楚。在这项研究中，我们研究了在模拟关节腔的环境中，将膝关节OA患者的SF添加到培养的用于治疗的ADSCs中的效果。添加SF后，观察到ADSCs的活力增加。利用DNA微阵列对sf处理的ADSCs进行基因表达谱分析，揭示了参与细胞存活的几个基因的变化。在这些基因中，我们重点研究了FOSL1，它参与了ADSCs的治疗效果和癌症干细胞的存活和增殖。我们分别通过RT-PCR和western blot分析证实了FOSL1 mRNA和蛋白的表达上调。接下来，我们使用siRNA敲除ADSCs中的FOSL1，观察到细胞活力下降，表明FOSL1参与了ADSCs的存活。有趣的是，在敲除的细胞中，SF暴露也降低了ADSC的活力。这些结果表明，SF通过上调FOSL1在ADSCs中的表达来增强细胞活力。对于使用培养的ADSCs进行治疗，如果能够建立一个更有利于ADSCs中FOSL1表达上调的环境，ADSCs的治疗效果可能会进一步增强。
Knee osteoarthritis (Knee OA) is an irreversible condition that causes bone deformity and degeneration of the articular cartilage that comprises the joints, resulting in chronic pain and movement disorders. The administration of cultured adipose-derived stem cells (ADSCs) into the knee joint cavity improves the clinical symptoms of Knee OA; however, the effect of synovial fluid (SF) filling the joint cavity on the injected ADSCs remains unclear. In this study, we investigated the effect of adding SF from Knee OA patients to cultured ADSCs prepared for therapeutic use in an environment that mimics the joint cavity. An increase in the viability of ADSCs was observed following the addition of SF. Gene expression profiling of SF-treated ADSCs using DNA microarrays revealed changes in several genes involved in cell survival. Of these genes, we focused on FOSL1, which is involved in the therapeutic effect of ADSCs and the survival and proliferation of cancer stem cells. We confirmed the upregulation of FOSL1 mRNA and protein expression using RT-PCR and western blot analysis, respectively. Next, we knocked down FOSL1 in ADSCs using siRNA and observed a decrease in cell viability, indicating the involvement of FOSL1 in the survival of ADSCs. Interestingly, in the knockdown cells, ADSC viability was also decreased by SF exposure. These results suggest that SF enhances cell viability by upregulating FOSL1 expression in ADSCs. For therapy using cultured ADSCs, the therapeutic effect of ADSCs may be further enhanced if an environment more conducive to the upregulation of FOSL1 expression in ADSCs can be established.
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