Model Animal Research Center, Jiangsu Key Laboratory of Molecular Medicine, Medical School, Nanjing University, Nanjing 210093, China.
Guangdong Institute of Intelligence Science and Technology, Hengqin, Zhuhai 519031, China.
Cells. 2024 Oct 28;13(21):1784. doi: 10.3390/cells13211784.
The intestines are in a constant state of motion and self-renewal. The mechanical breakdown of food facilitates intestinal movement and aids digestion. It is believed that mechanical stimulation, triggered by changes in osmotic pressure within the intestines, plays a crucial role in regulating gastrointestinal motility. While TRPs and PIEZO1/2 have been identified as mechanosensitive ion channels involved in this process, there still exist numerous unidentified channels with similar properties. In this study, we demonstrate that the TMEM63B expressed in intestinal stem cells contributes to the regulation of intestinal motility and digestion. The deletion of TMEM63B in intestinal stem cells not only decelerates intestinal motility and impairs digestion but also attenuates the proliferation of intestinal stem cells and exacerbates DSS-induced colitis in mice. Collectively, our findings unveil the pivotal role of TMEM63B in governing optimal digestive function and modulating intestinal motility.
肠道处于不断运动和自我更新的状态。食物的机械分解促进了肠道运动，有助于消化。人们认为，肠道内渗透压的变化引发的机械刺激在调节胃肠蠕动中起着至关重要的作用。虽然已经确定 TRP 和 PIEZO1/2 是参与该过程的机械敏感离子通道，但仍有许多具有相似特性的未识别通道。在这项研究中，我们证明了在肠干细胞中表达的 TMEM63B 有助于调节肠道蠕动和消化。肠干细胞中 TMEM63B 的缺失不仅会减缓肠道蠕动并损害消化，还会减弱肠干细胞的增殖，并在小鼠中加重 DSS 诱导的结肠炎。总之，我们的研究结果揭示了 TMEM63B 在控制最佳消化功能和调节肠道蠕动方面的关键作用。
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