The current knowledge of electrogenesis in mesenchymal stromal cells (MSCs) remains scarce. Earlier, we demonstrated that in MSCs from the human adipose tissue, transduction of certain agonists involved the phosphoinositide cascade. Its pivotal effector PLC generates DAG that can regulate ion channels directly or via its derivatives, including arachidonic acid (AA). Here we showed that AA strongly hyperpolarized MSCs by stimulating instantly activating, outwardly rectifying TEA-insensitive K⁺ channels. Among AA-regulated K⁺ channels, K2P channels from the TREK subfamily appeared to be an appropriate target. The expression of K2P channels in MSCs was verified by RT-PCR, which revealed TWIK-1, TREK-1, and TASK-5 transcripts. The TREK-1 inhibitor spadin antagonized the electrogenic action of AA, which was simulated by the channel activator BL 1249. This functional evidence suggested that TREK-1 channels mediated AA-dependent hyperpolarization of MSCs. Being mostly silent at rest, TREK-1 negligibly contributed to the “background” K⁺ current. The dramatic stimulation of TREK-1 channels by AA indicates their involvement in AA-dependent signaling in MSCs.

间充质基质细胞（MSCs）的电生成的当前知识仍然很少。之前，我们证明了在人类脂肪组织的MSC中，某些激动剂的转导涉及磷酸肌醇级联反应。它的关键效应器PLC生成DAG，DAG可以直接或通过其衍生物（包括花生四烯酸（AA））调节离子通道。在这里，我们通过刺激瞬间激活，向外纠正TEA不敏感的K ⁺通道，AA强烈强极化了MSC 。在AA管制的K ^+中渠道，TREK亚家族的K2P渠道似乎是合适的目标。通过RT-PCR验证了MSC中K2P通道的表达，揭示了TWIK-1，TREK-1和TASK-5转录本。TREK-1抑制剂spadin拮抗AA的电生成作用，这是由通道激活剂BL 1249模拟的。该功能证据表明TREK-1通道介导了MSC的AA依赖性超极化。TREK-1在静止时几乎保持沉默，对“背景” K ⁺电流的贡献微不足道。AA对TREK-1通道的剧烈刺激表明它们参与了MSC中AA依赖性信号传导。