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首页> 外文期刊>American Journal of Physiology >TNFR1 signaling resistance associated with female stem cell cytokine production is independent of TNFR2-mediated pathways.
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TNFR1 signaling resistance associated with female stem cell cytokine production is independent of TNFR2-mediated pathways.

机译：与女性干细胞细胞因子产生相关的TNFR1信号抗性独立于TNFR2介导的途径。

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摘要

End-organ ischemia is a common source of patient morbidity and mortality. Stem cell therapy represents a novel treatment modality for ischemic diseases and may aid injured tissues through the release of beneficial paracrine mediators. Female bone marrow mesenchymal stem cells (MSCs) have demonstrated a relative resistance to detrimental TNF receptor 1 (TNFR1) signaling and are thought to be superior to male stem cells in limiting inflammation. However, it is not known whether sex differences exist in TNF receptor 2 (TNFR2)-ablated MSCs. Therefore, we hypothesized that 1) sex differences would be observed in wild-type (WT) and TNFR2-ablated MSC cytokine signaling, and 2) the production of IL-6, VEGF, and IGF-1 in males, but not females, would be mediated through TNFR2. MSCs were harvested from male and female WT and TNFR2 knockout (TNFR2KO) mice and were subsequently exposed to TNF (50 ng/ml) or LPS (100 ng/ml). After 24 h, supernatants were collected and measured for cytokines. TNF and LPS stimulated WT stem cells to produce cytokines, but sex differences were only seen in IL-6 and IGF-1 after TNF stimulation. Ablation of TNFR2 increased VEGF and IGF-1 production in males compared with wild-type, but no difference was observed in females. Female MSCs from TNFR2KOs produced significantly lower levels of VEGF and IGF-1 compared with male TNFR2KOs. The absence of TNFR2 signaling appears to play a greater role in male MSC cytokine production. As a result, male, but not female stem cell cytokine production may be mediated through TNFR2 signaling cascades.
机译：终末器官缺血是患者发病和死亡的常见来源。干细胞疗法代表了一种针对缺血性疾病的新型治疗方式，并可能通过释放有益的旁分泌介质来帮助受伤的组织。雌性骨髓间充质干细胞（MSCs）已显示出对有害TNF受体1（TNFR1）信号的相对抗性，并被认为在限制炎症方面优于雄性干细胞。然而，尚不清楚在TNF受体2（TNFR2）消融的MSC中是否存在性别差异。因此，我们假设1）在野生型（WT）和TNFR2切除的MSC细胞因子信号传导中将观察到性别差异，并且2）在男性而非女性中会产生IL-6，VEGF和IGF-1，通过TNFR2介导。从雄性和雌性WT和TNFR2敲除（TNFR2KO）小鼠中收获MSC，然后将其暴露于TNF（50ng / ml）或LPS（100ng / ml）。 24小时后，收集上清液并测量细胞因子。 TNF和LPS刺激WT干细胞产生细胞因子，但仅在TNF刺激后在IL-6和IGF-1中观察到性别差异。与野生型相比，雄性TNFR2的切除增加了VEGF和IGF-1的产生，但在雌性中没有观察到差异。与男性TNFR2KO相比，来自TNFR2KO的女性MSC产生的VEGF和IGF-1水平显着降低。 TNFR2信号的缺失似乎在雄性MSC细胞因子产生中起着更大的作用。结果，可以通过TNFR2信号级联来介导雄性而不是雌性干细胞细胞因子的产生。

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