Webbläsaren som du använder stöds inte av denna webbplats. Alla versioner av Internet Explorer stöds inte längre, av oss eller Microsoft (läs mer här: * https://www.microsoft.com/en-us/microsoft-365/windows/end-of-ie-support).

Var god och använd en modern webbläsare för att ta del av denna webbplats, som t.ex. nyaste versioner av Edge, Chrome, Firefox eller Safari osv.

Differences in Origin of Reactive Microglia in Bone Marrow Chimeric Mouse and Rat After Transient Global Ischemia.

Författare

  • Kate L Lambertsen
  • Tomas Deierborg
  • Rikke Gregersen
  • Bettina H Clausen
  • Martin Wirenfeldt
  • Helle H Nielsen
  • Ishar Dalmau
  • Nils H Diemer
  • Frederik Dagnaes-Hansen
  • Flemming F Johansen
  • Armand Keating
  • Bente Finsen

Summary, in English

Current understanding of microglial involvement in disease is influenced by the observation that recruited bone marrow (BM)-derived cells contribute to reactive microgliosis in BM-chimeric mice. In contrast, a similar phenomenon has not been reported for BM-chimeric rats. We investigated the recruitment and microglial transformation of BM-derived cells in radiation BM-chimeric mice and rats after transientglobal cerebral ischemia, which elicits a characteristic microglialreaction. Both species displayed microglial hyperplasia and rod cell transformation in the hippocampal CA1 region. In mice, a subpopulation of lesion-reactive microglia originated from transformed BM-derived cells. By contrast, no recruitment or microglial transformation of BM-derived cells was observed in BM-chimeric rats. These results suggest that reactive microglia in rats originate from resident microglia, whereas they have a mixed BM-derived and resident origin in mice, depending on the severity of ischemic tissue damage.

Publiceringsår

2011

Språk

Engelska

Sidor

481-494

Publikation/Tidskrift/Serie

Journal of Neuropathology and Experimental Neurology

Volym

70

Issue

6

Dokumenttyp

Artikel i tidskrift

Förlag

American Association of Neuropathologists

Ämne

  • Neurology

Status

Published

ISBN/ISSN/Övrigt

  • ISSN: 1554-6578