transparent gif

 

Ej inloggad.

Göteborgs universitets publikationer

Complement peptide C3a promotes astrocyte survival in response to ischemia.

Författare och institution:
Noriko Shinjyo (Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering); Yolanda de Pablo (Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering); Milos Pekny (Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering); Marcela Pekna (Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering)
Publicerad i:
Molecular Neurobiology, 53 ( 5 ) s. 3076-87
ISSN:
0893-7648
Publikationstyp:
Artikel, refereegranskad vetenskaplig
Publiceringsår:
2016
Språk:
engelska
Fulltextlänk:
Sammanfattning (abstract):
Astrocytes are the most numerous cells in the central nervous system with a range of homeostatic and regulatory functions. Under normal conditions as well as after ischemia, astrocytes promote neuronal survival. We have previously reported that the complement-derived peptide C3a stimulates neuronal differentiation of neural progenitor cells and protects the immature brain tissue against hypoxic-ischemic injury. Here, we studied the effects of C3a on the response of mouse cortical astrocytes to ischemia. We have found that chemical ischemia, induced by combined inhibition of oxidative phosphorylation and glycolysis, upregulates the expression of C3a receptor in cultured primary astrocytes. C3a treatment protected wild-type but not C3a receptor-deficient astrocytes from cell death induced by chemical ischemia or oxygen-glucose deprivation by reducing ERK signaling and caspase-3 activation. C3a attenuated ischemia-induced upregulation of glial fibrillary acidic protein; however, the protective effects of C3a were not dependent on the presence of the astrocyte intermediate filament system. Pre-treatment of astrocytes with C3a during recovery abrogated the ischemia-induced neuroprotective phenotype of astrocytes. Jointly, these results provide the first evidence that the complement peptide C3a modulates the response of astrocytes to ischemia and increases their ability to cope with ischemic stress.
Ämne (baseras på Högskoleverkets indelning av forskningsämnen):
MEDICIN OCH HÄLSOVETENSKAP ->
Medicinska grundvetenskaper
Nyckelord:
Caspase-3, Glial fibrillary acidic protein, Neuroprotection
Postens nummer:
226706
Posten skapad:
2015-12-01 11:45
Posten ändrad:
2016-07-26 16:19

Visa i Endnote-format

Göteborgs universitet • Tel. 031-786 0000
© Göteborgs universitet 2007