Overexpression of the immunoreceptor CD300F has a neuroprotective role in a model of acute brain injury

Hugo Peluffo, Daniela Alí-Ruiz, Aroa Ejarque-Ortíz, Victor Heras-Alvarez, Emma Comas-Casellas, Agueda Martínez-Barriocanal, Andres Kamaid, Damiana Alvarez-Errico, Maria Luciana Negro, Natalia Lago, Simó Schwartz, Antonio Villaverde, Joan Sayós

Research output: Contribution to journalArticleResearchpeer-review

17 Citations (Scopus)

Abstract

It is well known that cell surface immune receptors play a critical role in regulating immune and inflammatory processes in the central nervous system (CNS). We have analyzed the function of cluster of differentiation (CD)300f immunoreceptor in a model of excitotoxic rat brain damage. First, to explore the presence of endogenous ligand(s) for this receptor we used a human CD300f-Ig soluble protein and confocal microscopy, showing specific staining mainly in CNS white matter and on the surface of oligodendrocytes and certain astrocytes. Next, we demonstrated in a model of in vivo rat brain excitotoxic damage that the overexpression of human CD300f induced a significant reduction in the lesion volume. To validate these results, we cloned the rat ortholog of CD300f protein (rCD300f). The overexpression of rCD300f receptor had a comparable neuroprotective effect after the acute brain injury and a similar CNS staining pattern when stained with the rCD300f-Ig soluble protein. Interestingly, when we analyzed the expression pattern of rCD300f in brain cells by quantitative polymerase chain reaction and immunohistochemistry, we detected the expression of CD300f as expected in microglial cells, but also in oligodendrocytes and neurons. These data suggest that the neuroprotective role of CD300f would be the result of a complex network of cell interactions. © 2011 The Authors; © 2011 International Society of Neuropathology.
Original languageEnglish
Pages (from-to)318-328
JournalBrain Pathology
Volume22
Issue number3
DOIs
Publication statusPublished - 1 May 2012

Keywords

  • Excitotoxicity
  • Inflammation
  • Microglia
  • Neuroprotection
  • Nonviral gene therapy
  • Oligodendrocyte

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