An extended window of opportunity for G-CSF treatment in cerebral ischemia
<p>Abstract</p> <p>Background</p> <p>Granulocyte-colony stimulating factor (G-CSF) is known as a powerful regulator of white blood cell proliferation and differentiation in mammals. We, and others, have shown that G-CSF is effective in treating cerebral ischemia in rode...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
BMC
2006-10-01
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| Series: | BMC Biology |
| Online Access: | http://www.biomedcentral.com/1741-7007/4/36 |
| _version_ | 1818915472102391808 |
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| author | Schwab Stefan Laage Rico Krüger Carola Pitzer Claudia Wysocki Rainer Schneider Armin Bach Alfred Schäbitz Wolf-Rüdiger |
| author_facet | Schwab Stefan Laage Rico Krüger Carola Pitzer Claudia Wysocki Rainer Schneider Armin Bach Alfred Schäbitz Wolf-Rüdiger |
| author_sort | Schwab Stefan |
| collection | DOAJ |
| description | <p>Abstract</p> <p>Background</p> <p>Granulocyte-colony stimulating factor (G-CSF) is known as a powerful regulator of white blood cell proliferation and differentiation in mammals. We, and others, have shown that G-CSF is effective in treating cerebral ischemia in rodents, both relating to infarct size as well as functional recovery. G-CSF and its receptor are expressed by neurons, and G-CSF regulates apoptosis and neurogenesis, providing a rational basis for its beneficial short- and long-term actions in ischemia. In addition, G-CSF may contribute to re-endothelialisation and arteriogenesis in the vasculature of the ischemic penumbra. In addition to these trophic effects, G-CSF is a potent neuroprotective factor reliably reducing infarct size in different stroke models.</p> <p>Results</p> <p>Here, we have further delayed treatment and studied effects of G-CSF on infarct volume in the middle cerebral artery occlusion (MCAO) model and functional outcome in the cortical photothrombotic model. In the MCAO model, we applied a single dose of 60 μg/kg bodyweight G-CSF in rats 4 h after onset of ischemia. Infarct volume was determined 24 h after onset of ischemia. In the rat photothrombotic model, we applied 10 μg/kg bodyweight G-CSF daily for a period of 10 days starting either 24 or 72 h after induction of ischemia. G-CSF both decreased acute infarct volume in the MCAO model, and improved recovery in the photothrombotic model at delayed timepoints.</p> <p>Conclusion</p> <p>These data further strengthen G-CSF's profile as a unique candidate stroke drug, and provide an experimental basis for application of G-CSF in the post-stroke recovery phase.</p> |
| first_indexed | 2024-12-20T00:02:49Z |
| format | Article |
| id | doaj.art-3ca86c3d6686473686bd4ecf69aa4234 |
| institution | Directory Open Access Journal |
| issn | 1741-7007 |
| language | English |
| last_indexed | 2024-12-20T00:02:49Z |
| publishDate | 2006-10-01 |
| publisher | BMC |
| record_format | Article |
| series | BMC Biology |
| spelling | doaj.art-3ca86c3d6686473686bd4ecf69aa42342022-12-21T20:00:45ZengBMCBMC Biology1741-70072006-10-01413610.1186/1741-7007-4-36An extended window of opportunity for G-CSF treatment in cerebral ischemiaSchwab StefanLaage RicoKrüger CarolaPitzer ClaudiaWysocki RainerSchneider ArminBach AlfredSchäbitz Wolf-Rüdiger<p>Abstract</p> <p>Background</p> <p>Granulocyte-colony stimulating factor (G-CSF) is known as a powerful regulator of white blood cell proliferation and differentiation in mammals. We, and others, have shown that G-CSF is effective in treating cerebral ischemia in rodents, both relating to infarct size as well as functional recovery. G-CSF and its receptor are expressed by neurons, and G-CSF regulates apoptosis and neurogenesis, providing a rational basis for its beneficial short- and long-term actions in ischemia. In addition, G-CSF may contribute to re-endothelialisation and arteriogenesis in the vasculature of the ischemic penumbra. In addition to these trophic effects, G-CSF is a potent neuroprotective factor reliably reducing infarct size in different stroke models.</p> <p>Results</p> <p>Here, we have further delayed treatment and studied effects of G-CSF on infarct volume in the middle cerebral artery occlusion (MCAO) model and functional outcome in the cortical photothrombotic model. In the MCAO model, we applied a single dose of 60 μg/kg bodyweight G-CSF in rats 4 h after onset of ischemia. Infarct volume was determined 24 h after onset of ischemia. In the rat photothrombotic model, we applied 10 μg/kg bodyweight G-CSF daily for a period of 10 days starting either 24 or 72 h after induction of ischemia. G-CSF both decreased acute infarct volume in the MCAO model, and improved recovery in the photothrombotic model at delayed timepoints.</p> <p>Conclusion</p> <p>These data further strengthen G-CSF's profile as a unique candidate stroke drug, and provide an experimental basis for application of G-CSF in the post-stroke recovery phase.</p>http://www.biomedcentral.com/1741-7007/4/36 |
| spellingShingle | Schwab Stefan Laage Rico Krüger Carola Pitzer Claudia Wysocki Rainer Schneider Armin Bach Alfred Schäbitz Wolf-Rüdiger An extended window of opportunity for G-CSF treatment in cerebral ischemia BMC Biology |
| title | An extended window of opportunity for G-CSF treatment in cerebral ischemia |
| title_full | An extended window of opportunity for G-CSF treatment in cerebral ischemia |
| title_fullStr | An extended window of opportunity for G-CSF treatment in cerebral ischemia |
| title_full_unstemmed | An extended window of opportunity for G-CSF treatment in cerebral ischemia |
| title_short | An extended window of opportunity for G-CSF treatment in cerebral ischemia |
| title_sort | extended window of opportunity for g csf treatment in cerebral ischemia |
| url | http://www.biomedcentral.com/1741-7007/4/36 |
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