Integrated RNA-Seq Profiling Identifies NRXN1+ Cell-Fibroblast Associated MAPK Signaling in Prurigo Nodularis.
6 affiliations
- 1Department of Biomedical Science, Seoul National University College of Medicine, Seoul, Korea.
- 2Genomic Medicine Institute, Medical Research Center, Seoul National University, Seoul, Korea.
- 3Department of Dermatology, College of Medicine, The Catholic University of Korea, Seoul, Korea.
- 4Department of Dermatology, National Medical Center, Seoul, Korea.
- 5Genomic Medicine Institute, Medical Research Center, Seoul National University, Seoul, Korea. [email protected].
- 6Department of Dermatology, National Medical Center, Seoul, Korea. [email protected].
Abstract
Purpose
Prurigo nodularis (PN) is chronic pruritic dermatosis with hyperkeratotic nodules and persistent itch, occurring alone or with atopic dermatitis (AD). The molecular basis of nodular architecture and sustained pruritus remain poorly defined, particularly the role of fibroblasts and their interactions with neuronal components. This study aimed to identify PN-specific pathogenic profiles by comparing lesional transcriptomes from AD, atopic prurigo (AP), and PN.Methods
Bulk RNA sequencing was performed on lesional skin from AD (n = 6), AP (n = 7), PN (n = 7), and healthy controls (HC; n = 4). Publicly available single-cell RNA-sequencing datasets were reanalyzed for cell-type signatures. Integrated analyses included differentially expressed genes, pathway enrichment, cell-type deconvolution, ligand-receptor inference, and immune cell profiling.Results
PN lesions showed MAPK/ERK pathway enrichment in fibroblasts compared with AD and AP. NRXN1+ cells were inferred as major interacting partners of fibroblasts, with ligand-receptor interactions consistent with enhanced fibroblast MAPK/ERK activity. Immune pathway analyses showed weaker Th2 pathway activity in PN compared with AD/AP, providing context for neuronal-stromal interactions as a putative distinguishing feature.Conclusions
PN shows enhanced MAPK/ERK pathway enrichment in fibroblasts and inferred NRXN1+ cell-fibroblast interactions. This candidate axis may contribute to nodular lesion architecture and persistent pruritus, suggesting potential therapeutic strategies.
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BibTeX
@article{jang2026integrated,
title = {{Integrated RNA-Seq Profiling Identifies NRXN1+ Cell-Fibroblast Associated MAPK Signaling in Prurigo Nodularis.}},
author = {Jiyun Jang and Young-Bok Lee and Hwee-Seon Park and Narang Hong and Hyung Don Kook and Hye Jung Jung and Jong-Il Kim and Jiyoung Ahn},
journal = {Allergy, asthma \& immunology research},
year = {2026},
month = sep,
doi = {10.4168/aair.2026.18.5.761},
url = {https://europepmc.org/article/MED/42845230},
note = {CC BY-NC},
}
RIS
TY - JOUR
TI - Integrated RNA-Seq Profiling Identifies NRXN1+ Cell-Fibroblast Associated MAPK Signaling in Prurigo Nodularis.
AU - Jiyun Jang
AU - Young-Bok Lee
AU - Hwee-Seon Park
AU - Narang Hong
AU - Hyung Don Kook
AU - Hye Jung Jung
AU - Jong-Il Kim
AU - Jiyoung Ahn
PY - 2026
DA - 2026/09/01
JO - Allergy, asthma & immunology research
DO - 10.4168/aair.2026.18.5.761
UR - https://europepmc.org/article/MED/42845230
AB - Purpose Prurigo nodularis (PN) is chronic pruritic dermatosis with hyperkeratotic nodules and persistent itch, occurring alone or with atopic dermatitis (AD). The molecular basis of nodular architecture and sustained pruritus remain poorly defined, particularly the role of fibroblasts and their interactions with neuronal components. This study aimed to identify PN-specific pathogenic profiles by comparing lesional transcriptomes from AD, atopic prurigo (AP), and PN.Methods Bulk RNA sequencing was performed on lesional skin from AD (n = 6), AP (n = 7), PN (n = 7), and healthy controls (HC; n = 4). Publicly available single-cell RNA-sequencing datasets were reanalyzed for cell-type signatures. Integrated analyses included differentially expressed genes, pathway enrichment, cell-type deconvolution, ligand-receptor inference, and immune cell profiling.Results PN lesions showed MAPK/ERK pathway enrichment in fibroblasts compared with AD and AP. NRXN1+ cells were inferred as major interacting partners of fibroblasts, with ligand-receptor interactions consistent with enhanced fibroblast MAPK/ERK activity. Immune pathway analyses showed weaker Th2 pathway activity in PN compared with AD/AP, providing context for neuronal-stromal interactions as a putative distinguishing feature.Conclusions PN shows enhanced MAPK/ERK pathway enrichment in fibroblasts and inferred NRXN1+ cell-fibroblast interactions. This candidate axis may contribute to nodular lesion architecture and persistent pruritus, suggesting potential therapeutic strategies.
SN - 2092-7355
SN - 2092-7363
ER -