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Cerebral ischemia-reperfusion induces the expression of phoenixin receptor (GPR173) and adult neurogenesis marker proteins in the rat striatum

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E-pub ahead of print
  • Kinga Mordecka-Chamera
  • Artur Pałasz
  • Aleksandra Suszka-Świtek
  • Katarzyna Bogus
  • Władysław Skałba
  • Aneta Piwowarczyk-Nowak
  • John J. Worthington
  • Marta Pukowiec
  • Veerta Sharma
  • Łukasz Filipczyk
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<mark>Journal publication date</mark>12/05/2025
<mark>Journal</mark>Brain Injury
Issue number6
Volume39
Number of pages7
Pages (from-to)457-463
Publication StatusE-pub ahead of print
Early online date29/12/24
<mark>Original language</mark>English

Abstract

Objective
Brain ischemia is considered an extremely potent stress factor at the cellular and molecular level which may lead to massive neuronal death. Alternatively, short brain ischemia and reperfusion (I/R) can actually stimulate neurogenesis, angiogenesis and peptidergic signaling. There is little known about the potential effect of I/R on brain expression of the novel neuropeptide; phoenixin (PNX) and its receptor GPR173.

Methods
The study was carried out on adult male Wistar rats divided into seven groups: control, sham operation and 5 ischemic experimental groups across the time course of reperfusion. We examined mRNA and protein expression of GPR173 and neurogenesis markers Musashi-1, doublecortin (DCX), and Sox-2 in the striatum.

Results
GPR-173 positive cells were found only in the ischemic hemisphere, where Musashi-1, DCX and Sox-2-positive cells were also observed. Gene expression analysis also showed a significant increase of GPR-173 mRNA level in the I/R striatum in comparison with the control one. Results confirm previous findings suggesting that I/R stimulates adult neurogenesis in the striatum and affects peptidergic signaling in this structure.

Conclusions
A very fast occurence of GPR-173 expression revealed in the striatum may potentially be exclusively related to neuroprotective neurochemical changes that occur in this region after I/R.