Presentation: Activin a receptor 1C may implicate in the development of sensitive skin ( World Allergy Congress)

Wednesday, 14 October 2015

Hall D1 Foyer (Floor 3) (Coex Convention Center)

Eun Ju Kim, PhD , Department of Dermatology, Seoul National University Hospital, Seoul, South Korea

Dong Hun Lee, MD, PhD , Department of Dermatology, Seoul National University Hospital, Seoul, South Korea

Yeon Kyung Kim , Department of Dermatology, Seoul National University Hospital, Seoul, South Korea

Eun Jin Doh, MD , Department of Dermatology, Seoul National University Hospital, Seoul, South Korea

Seon Pil Jin , Department of Dermatology, Seoul National University Hospital, Seoul, South Korea

Young Mee Lee, PhD , Department of Dermatology, Seoul National University Hospital, Seoul, South Korea

Hee Chul Eun, MD PhD , Department of Dermatology, Seoul National University Hospital, Seoul, South Korea

Jin Ho Chung, MD PhD , Department of Dermatology, Seoul National University Hospital, Seoul, South Korea

Background: Sensitive skin is a hyperactive skin condition characterized by sensory symptoms showing exaggerated reactions in response to internal stimulants and external irritants. Recently, using microarray-driven approach, we found that several signaling pathway regulated genes including activin A receptor 1C (ACVR1C) were down-regulated in sensitive skin. ACVR1C, a type I serine/threonine kinase receptor for the transforming growth factor (TGF)-β family, is activated by various ligands such as nodal, activin B.

Methods: In this study, we investigate the roles of ACVR1C in the pathogenesis of skin hypersensitivity using an in vitro model as well as human skin.

Results: ACVR1C mRNA and protein expressions were significantly decreased in sensitive skin compared with non-sensitive skin. A decreased level of pH in sensitive skin can induce an increase of calcium influx through transient receptor potential cation channel subfamily V member 1 (TRPV1). Indeed, sensitive skin showed excessive calcium accumulation as compared with non-sensitive skin. RD cells transfected with ACVR1C siRNA exhibited markedly enhanced responses in intracellular Ca²⁺ concentration following calcium ionophore treatment. Furthermore, knockdown of ACVR1C induced the expression of TRPV1 and calcitonin gene-related peptide (CGRP) indicating the causative role of ACVR1C in the pathogenesis of pain in sensitive skin. Finally, we investigated whether stimulation of ACVR1C pathway has a therapeutic potential to alleviate sensitive skin. Intriguingly, treatment of RD cells with Nodal induced a substantial reduction in the Ca²⁺ influx and the expression of TRPV1 and CGRP which was increased by knockdown of ACVR1C, supporting the possible therapeutic role of ACVR1C stimulation in sensitive skin.

Conclusions: Taken together, our results demonstrate that ACVR1C play crucial roles in the pathogenesis of sensitive skin and the activation of these signaling pathways in vitro successfully reversed pain sensation in RD cells, thereby raising the possibility of a novel therapeutic approach for skin hypersensitivity.

1080 Activin a receptor 1C may implicate in the development of sensitive skin