Fibroblast-directed melanocyte recruitment via Cxcl12-Cxcr4 cascade promotes post-inflammatory hyperpigmentation and skin barrier protection in zebrafish
Ontology highlight
ABSTRACT: Post-inflammatory hyperpigmentation (PIH), a prevalent dermatological condition, is classically attributed to melanocyte overactivation in situ. However, the precise triggers and physiological significance of melanocyte responses remain elusive. Using an acetic acid corrosion-induced zebrafish PIH model, here we demonstrate that melanocyte migration to the inflammatory site is a key pathogenic driver of hyperpigmentation. This migration is largely orchestrated by fibroblasts, but not macrophages or neutrophils, which secrete the chemokine cxcl12a upon injury, recruiting melanocytes via the cxcl12a-cxcr4a signaling axis. Beyond hyperpigmentation, we reveal that melanocytes function as a dual protective barrier against both UV-induced DNA damage and microbial invasion in response to acetic acid corrosion-induced injury. Our findings provide new insights into PIH pathogenesis and uncover the non-canonical barrier functions of melanocytes in skin inflammation and repair.
ORGANISM(S): Danio rerio
PROVIDER: GSE302529 | GEO | 2025/10/01
REPOSITORIES: GEO
ACCESS DATA