List of Publications (2011-Current)
2026
Kim, Yejoon; Choi, Junhyeok; Kim, Minjun; Rawal, Diwas; Lee, Wook-Joo; Shim, Won-Sik
Vitexin alleviates atopic dermatitis–associated itch via TRPV4 inhibition in sensory neurons and MRGPRX2/MrgprB2 blockade in mast cells Journal Article
In: International Immunopharmacology, vol. 168, 2026, ISSN: 1567-5769.
Abstract | Links | BibTeX | Tags: Atopic dermatitis, Itch, Mast cell, MrgprB2, MRGPRX2, Sensory neurons, TRPV4
@article{Kim2026,
title = {Vitexin alleviates atopic dermatitis–associated itch via TRPV4 inhibition in sensory neurons and MRGPRX2/MrgprB2 blockade in mast cells},
author = {Yejoon Kim and Junhyeok Choi and Minjun Kim and Diwas Rawal and Wook-Joo Lee and Won-Sik Shim},
doi = {10.1016/j.intimp.2025.115757},
issn = {1567-5769},
year = {2026},
date = {2026-01-00},
urldate = {2026-01-00},
journal = {International Immunopharmacology},
volume = {168},
publisher = {Elsevier BV},
abstract = {Chronic itch is a debilitating symptom in atopic dermatitis (AD), often resistant to current antipruritic therapies. Here, we demonstrate that vitexin (VTX) exerts antipruritic effects through modulation of neuronal and mast cell pathways. Calcium imaging in TRPV4-transfected HEK293T cells and primary mouse dorsal root ganglion neurons demonstrated that VTX substantially inhibited TRPV4-dependent calcium influx, reducing both peak responses and the proportion of agonist-responsive neurons. Parallel assays in HEK293T cells expressing human MRGPRX2 and murine MrgprB2 revealed dose-dependent suppression of compound 48/80-induced calcium signaling. Mast-cell degranulation assays indicated that VTX markedly decreased β-hexosaminidase release from primary mouse peritoneal mast cells and HMC1.2 cells upon compound 48/80 stimulation. In silico molecular docking analysis showed that VTX occupied overlapping binding regions with known agonists in TRPV4 and MRGPRX2/MrgprB2, suggesting direct receptor interactions. In an MC903-induced murine model of AD, VTX reduced scratching behavior, mast cell activation, and transcriptional upregulation of Trpv4 and MrgprB2. Notably, antipruritic effects were enhanced in Trpv4-deficient mice, indicating the contribution of MRGPRX2/MrgprB2 suppression. These findings identify VTX as a promising antipruritic candidate for AD-associated pruritus, and mechanistic insights provide a rationale for further exploration of VTX in advanced AD models and eventual translation to clinical therapies.},
keywords = {Atopic dermatitis, Itch, Mast cell, MrgprB2, MRGPRX2, Sensory neurons, TRPV4},
pubstate = {published},
tppubtype = {article}
}
Chronic itch is a debilitating symptom in atopic dermatitis (AD), often resistant to current antipruritic therapies. Here, we demonstrate that vitexin (VTX) exerts antipruritic effects through modulation of neuronal and mast cell pathways. Calcium imaging in TRPV4-transfected HEK293T cells and primary mouse dorsal root ganglion neurons demonstrated that VTX substantially inhibited TRPV4-dependent calcium influx, reducing both peak responses and the proportion of agonist-responsive neurons. Parallel assays in HEK293T cells expressing human MRGPRX2 and murine MrgprB2 revealed dose-dependent suppression of compound 48/80-induced calcium signaling. Mast-cell degranulation assays indicated that VTX markedly decreased β-hexosaminidase release from primary mouse peritoneal mast cells and HMC1.2 cells upon compound 48/80 stimulation. In silico molecular docking analysis showed that VTX occupied overlapping binding regions with known agonists in TRPV4 and MRGPRX2/MrgprB2, suggesting direct receptor interactions. In an MC903-induced murine model of AD, VTX reduced scratching behavior, mast cell activation, and transcriptional upregulation of Trpv4 and MrgprB2. Notably, antipruritic effects were enhanced in Trpv4-deficient mice, indicating the contribution of MRGPRX2/MrgprB2 suppression. These findings identify VTX as a promising antipruritic candidate for AD-associated pruritus, and mechanistic insights provide a rationale for further exploration of VTX in advanced AD models and eventual translation to clinical therapies.