Mas-related G protein-coupled receptor D is involved in modulation of murine gastrointestinal motility.
Mas-related G protein-coupled receptor D is involved in modulation of murine gastrointestinal motility.
复制标题
Mas 相关的 G 蛋白偶联受体 D 参与小鼠胃肠运动的调节。
DOI：
10.1113/ep089958
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发表时间：
2021
影响因子：
2.7
通讯作者：
Lei Lan
中科院分区：
文献类型：
--
作者：
Min Xu;Jia Li;Zhudi Zhang;Lin Liu;Fengyi Wan;Zongxiang Tang;Lei Lan
新发现本研究的中心问题是什么？Mas相关G蛋白偶联受体D（MrgprD）在胃肠运动中的生理功能尚不清楚。本研究的目的是评估MrgprD及其受体激动剂对小鼠胃肠动力的影响，主要发现及其重要性是什么？mrgprd缺乏可改善小鼠在体胃肠运动，但对小鼠在体肠环自发性收缩无影响。全身性给予MrgprD配体β-丙氨酸或alamandine，可延迟体内胃肠转运，减弱离体肠环的自发性收缩vivo.AbstractMas相关G蛋白偶联受体D（MrgprD）首先在小鼠背根神经节感觉神经元中被发现，并已被证明参与疼痛和瘙痒的感觉。虽然最近在胃肠道（GI）中发现了MrgprD的表达，但其在GI运动中的生理作用尚不清楚。为了解决这个问题，我们使用Mrgprd基因敲除（Mrgprd-/-）小鼠和MrgprD激动剂，分别研究Mrgprd基因缺失和MrgprD信号转导激活对小鼠肠道运动的影响，包括体内和体外。我们观察到Mrgprd的缺失加速了活性炭通过小鼠胃肠道的传输。但Mrgprd缺乏对Ileumex在体自发收缩的平均幅度和频率没有影响。近端和远端结肠的结肠运动复合体记录了野生型和Mrgprd −/−小鼠，但它们的对照频率没有差异。此外，在野生型小鼠中，全身施用MrgprD激动剂（β-丙氨酸或alamandine）在体内延迟GI转运，并在体内结肠中抑制回肠和结肠运动复合体的自发性收缩。我们的研究结果表明，MrgprD及其激动剂参与调节胃肠道运动的小鼠。
New FindingsWhat is the central question of this study?The physiological function of Mas‐related G protein‐coupled receptor D (MrgprD) in gastrointestinal motility is unknown. The aim of this study was to assess the effects of MrgprD and its receptor agonists on murine gastrointestinal motility.What is the main finding and its importance?Mrgprddeficiency improved murine gastrointestinal motility in vivo but had no effects on the spontaneous contractions of murine intestinal ringsex vivo. Systemic administration of the MrgprD ligand, either β‐alanine or alamandine, delayed gastrointestinal transit in vivo and attenuated the spontaneous contractions of isolated intestinal ringsex vivo.AbstractMas‐related G protein‐coupled receptor D (MrgprD) was first identified in sensory neurons of mouse dorsal root ganglion and has been demonstrated to be involved in sensations of pain and itch. Although expression of MrgprD has recently been found in the gastrointestinal (GI) tract, its physiological role in GI motility is unknown. To address this question, we usedMrgprdknockout (Mrgprd−/−) mice and MrgprD agonists to examine the effects ofMrgprdgene deletion and MrgprD signalling activation, respectively, on murine intestinal motility, both in vivo andex vivo. We observed that the deletion ofMrgprdaccelerated the transmission of charcoal through the mouse GI tract. ButMrgprddeficiency did not affect the mean amplitudes and frequencies of spontaneous contractions in ileumex vivo. Colonic motor complexes in the proximal and the distal colon were recorded from wild‐type andMrgprd−/−mice, but their control frequencies were not different. Moreover, in wild‐type mice, systemic administration of an MrgprD agonist, either β‐alanine or alamandine, delayed GI transit in vivo and suppressed spontaneous contractions in the ileum and colonic motor complexes in the colonex vivo. Our results suggest that MrgprD and its agonist are involved in the modulation of GI motility in mice.