PUBLICATION

Stay or Stray: Lpar1 regulates neutrophil retention and epidermal homeostasis in early zebrafish development

Authors
Li, S.C., Lin, Y.C., Hsiao, C.D., Lee, S.J.
ID
ZDB-PUB-251211-6
Date
2025
Source
Developmental Biology : (Journal)
Registered Authors
Hsiao, Chung-Der, Lee, Shyh-Jye
Keywords
Zebrafish, caudal hematopoietic tissue, chemokine (C-X-C motif) ligand 12a (Cxcl12a), lysophosphatidic acid receptor 1 (Lpar1), neutrophils
MeSH Terms
  • Animals
  • Apoptosis
  • Cell Movement
  • Chemokine CXCL12
  • Embryo, Nonmammalian
  • Epidermis*/embryology
  • Epidermis*/metabolism
  • Gene Expression Regulation, Developmental
  • Homeostasis*
  • Neutrophils*/cytology
  • Neutrophils*/metabolism
  • Neutrophils*/physiology
  • Receptors, Lysophosphatidic Acid*/genetics
  • Receptors, Lysophosphatidic Acid*/metabolism
  • Signal Transduction
  • Zebrafish*/embryology
  • Zebrafish*/genetics
  • Zebrafish*/metabolism
  • Zebrafish Proteins*/genetics
  • Zebrafish Proteins*/metabolism
PubMed
41371569 Full text @ Dev. Biol.
Abstract
Neutrophils play essential roles in host defense, but the mechanisms governing their developmental distribution remain poorly understood. Here, we identify a previously unrecognized function of lysophosphatidic acid receptor 1 (Lpar1) in maintaining neutrophil retention during early zebrafish development. Contrary to its previously described pro-inflammatory role, Lpar1 acts in an anti-inflammatory manner by preventing premature neutrophil dispersal. Mechanistically, Lpar1 regulates the expression of cxcl12a in the caudal hematopoietic tissue (CHT), establishing a novel Lpar1-Cxcl12a signaling axis that governs neutrophil localization. Lpar1 also influences neutrophil mobility through its effects on vascular integrity in the CHT, which is severely disrupted in Lpar1 morphants but may be mildly affected in Lpar1 mutants. Dispersed neutrophils are predominantly recruited to the superficial epidermal layer, where numerous apoptotic cells are present. Collectively, these findings refine current models of immune regulation during development and reveal an alternative mechanism that may contribute to the development of inflammatory skin disorders.
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Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping