MRGPRD

Last update 08 May 2025

Basic Info

Synonyms

Beta-alanine receptor, G-protein coupled receptor TGR7, MAS related GPR family member D

+ [4]

Introduction

May regulate nociceptor function and/or development, including the sensation or modulation of pain. Functions as a specific membrane receptor for beta-alanine. Beta-alanine at micromolar doses specifically evoked Ca(2+) influx in cells expressing the receptor. Beta-alanine decreases forskolin-stimulated cAMP production in cells expressing the receptor, suggesting that the receptor couples with G-protein G(q) and G(i).

100 Clinical Results associated with MRGPRD

100 Translational Medicine associated with MRGPRD

0 Patents (Medical) associated with MRGPRD

164

Literatures (Medical) associated with MRGPRD

01 May 2025·Arteriosclerosis, Thrombosis, and Vascular Biology

MrgD as a Novel Modeling and Treatment Target for Pulmonary Hypertension

Article

Author: Wang, Qianqian ; Liu, Xiaolin ; Zhang, Cheng ; Yao, Lina ; Zhang, Yun ; Zhong, Hongyu ; Liu, Dongdong ; Hao, Panpan ; Zhang, Mei ; An, Huailong ; Fang, Lijun ; Fan, Cong ; Li, Qimou

BACKGROUND:The hyperproliferation of smooth muscle cells and deposition of collagen in the pulmonary artery are among the primary characteristics of pulmonary hypertension (PH). These processes contribute to vascular remodeling, ultimately leading to elevated pulmonary artery pressure and right ventricular failure. The MrgD (Mas-related G-protein–coupled receptor member D) exhibits close associations with certain cardiovascular diseases; however, its role in PH remains unclear.METHODS:The effects of the absence or activation of MrgD on PH were investigated using PH animal models induced by Sugen5416+hypoxia, monocrotaline, as well as global or smooth muscle–specific knockout of MrgD. Signaling pathways regulated by MrgD were investigated using high-throughput screening of data from single-cell sequencing of mouse lungs and RNA sequencing of human pulmonary artery smooth muscle cells, as well as other molecular biology experiments.RESULTS: We observed decreased MrgD levels in animal models and patients with PH. Both global and conditional knockout of MrgD exacerbated hypoxia-induced PH in mice. MrgD activation attenuated the PH phenotypes in several established models, although these protective effects were reversed in MrgD-knockout mice. Transcriptome analysis revealed a significantly differentially expressed gene, PIM1 (proviral integration site for Moloney murine leukemia virus 1), as a potential MrgD target. Silencing MrgD increased pulmonary artery smooth muscle cell proliferation by facilitating the AKT (protein kinase B)-mediated interaction of MAZ (MYC-associated Zinc-finger protein) with PIM1 . MrgD activation inhibited this pathway and was ineffective in PH mice with pulmonary artery smooth muscle cells overexpressing PIM1. CONCLUSIONS:MrgD deficiency in pulmonary arterioles increases susceptibility to PH, particularly in a hypoxic environment. MrgD is a potential modeling and therapeutic target for PH.

04 Apr 2025·Science

Meningeal regulatory T cells inhibit nociception in female mice

Article

Author: Benitez, Jorge ; Pintar, John E. ; Kochhar, Nathan P. ; Eckalbar, Walter L. ; Domingos, Ana I. ; Braz, Joao M. ; Midavaine, Élora ; Rodriguez, Sian R. ; Moraes, Beatriz C. ; Basbaum, Allan I. ; Tian, Lin ; Kashem, Sakeen W.

T cells have emerged as orchestrators of pain amplification, but the mechanism by which T cells control pain processing is unresolved. We found that regulatory T cells (T reg cells) could inhibit nociception through a mechanism that was not dependent on their ability to regulate immune activation and tissue repair. Site-specific depletion or expansion of meningeal T reg cells (mT reg cells) in mice led to female-specific and sex hormone–dependent modulation of mechanical sensitivity. Specifically, mT reg cells produced the endogenous opioid enkephalin that exerted an antinociceptive action through the delta opioid receptor expressed by MrgprD + sensory neurons. Although enkephalin restrains nociceptive processing, it was dispensable for T reg cell–mediated immunosuppression. Thus, our findings uncovered a sexually dimorphic immunological circuit that restrains nociception, establishing T reg cells as sentinels of pain homeostasis.

01 Apr 2025·American Journal of Respiratory Cell and Molecular Biology

MrgprC11⁺ Jugular Neurons Control Airway Hyperresponsiveness in Allergic Airway Inflammation

Article

Author: Hancock, William ; Xing, Yanyan ; Nho, Yeseul ; Zhu, Yuyan ; Chang, Margaret Y. ; Han, Liang ; Lawson, Katy ; Ellison, Alexandra E.

The lung is densely innervated by sensory nerves, the majority of which are derived from the vagal sensory neurons. Vagal ganglia consist of two different ganglia, termed nodose and jugular ganglia, with distinct embryonic origins, innervation patterns, and physiological functions in the periphery. Because nodose neurons constitute the majority of the vagal ganglia, our understanding of the function of jugular nerves in the lung is very limited. This study aims to investigate the role of MrgprC11⁺ jugular sensory neurons in a mouse allergic asthma model. Our previous study has shown that MrgprC11⁺ jugular neurons mediate cholinergic bronchoconstriction. In this study, we found that, in addition to MrgprC11, several other Mrgpr family members, including MrgprA3, MrgprB4, and MrgprD, are also specifically expressed in the jugular sensory neurons. MrgprC11⁺ jugular neurons exhibit dense innervation in the respiratory tract, including the larynx, trachea, proximal bronchus, and distal bronchus. We also found that receptors for IL-4 and oncostatin M, two critical cytokines promoting allergic airway inflammation, are mainly expressed in jugular sensory neurons. Both IL-4 and oncostatin M can sensitize the neuronal responses of MrgprC11⁺ jugular neurons. Moreover, ablation of MrgprC11⁺ neurons significantly inhibited airway hyperresponsiveness in the asthmatic lung, demonstrating the critical role of MrgprC11⁺ neurons in controlling airway constriction. Our results emphasize the critical role of jugular sensory neurons in respiratory diseases and present MrgprC11⁺ neurons as a potential therapeutic target for treating airway hyperresponsiveness.

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MRGPRD

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