ZFIN ID: ZDB-PUB-100202-3
Prokineticin 2 expression is associated with neural repair of injured adult zebrafish telencephalon
Ayari, B., El Hachimi, K.H., Yanicostas, C., Landoulsi, A., and Soussi-Yanicostas, N.
Date: 2010
Source: Journal of neurotrauma   27(5): 959-972 (Journal)
Registered Authors: Soussi-Yanicostas, Nadia
Keywords: adult brain injury, models of injury, neural injury, regeneration, surgery
MeSH Terms:
  • Animals
  • Biomarkers/metabolism
  • Brain Injuries/metabolism*
  • Brain Injuries/physiopathology
  • Brain Injuries/therapy*
  • Cell Movement/genetics
  • Cell Proliferation
  • Disease Models, Animal
  • Nerve Regeneration/genetics*
  • Neurogenesis/genetics
  • Neuronal Plasticity/genetics
  • Neuropeptides/biosynthesis*
  • Neuropeptides/genetics
  • Neuropeptides/physiology
  • Recovery of Function/genetics
  • Telencephalon/metabolism*
  • Telencephalon/pathology
  • Telencephalon/physiopathology
  • Zebrafish/metabolism*
  • Zebrafish/physiology
  • Zebrafish Proteins/biosynthesis*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/physiology
PubMed: 20102264 Full text @ J. Neurotrauma
Prokineticin 2 (Prok2) is a secreted protein that regulates diverse biological processes including olfactory bulb neurogenesis in adult mammals. However, its precise role in this process is as yet not fully understood. Because it is well known that adult teleost fish, including zebrafish, display an intense proliferative activity in several brain regions, we took advantage of this feature to analyze the distribution of prok2 transcripts in the adult zebrafish brain and during injury-induced telencephalon (TC) regeneration. First, we characterized the zebrafish prok2 gene and showed that its transcription takes place in almost all proliferating areas previously identified in adult zebrafish brain. Moreover, in TC, prok2 transcription was mainly restricted to neurons. Next, using a novel model of TC injury in adult zebrafish, we observed that TC lesion induced a dramatic increase in cell proliferation within the injured hemisphere in regions located both adjacent and distal to injury sites. Moreover, our data strongly suggest that cell proliferation was followed by the migration of newly generated neurons towards injury sites. In addition, we observed a transient over-expression of prok2 transcripts, which was detected in cells surrounding the lesion during the very first days post-injury, and, a few days later, in broad cell rows extending from cortical regions of the TC toward injury site. prok2 over-expression was no longer detected when the regeneration process was close to completion, showing that ectopic prok2 transcription paralleled neuronal regeneration. Taken together, our results suggest that in adult zebrafish brain, Prok2 may play a role in both constitutive and injury-induced neurogenesis.