Abstract
We investigated the systemic effect of liposomes bearing apoptotic signals on the level of inflammation and neuronal death induced by ischemia-reperfusion (IR). Using a model of retinal ischemia, we showed that treatment with phosphatidylserine (PS) and phosphatidylcholine (PC) liposomes significantly reduced the expression of proinflammatory genes, including that of Il1b, Il6, Ccl2, Ccl5, Cxcl10, and Icam1, 24 h after reperfusion. Phosphatidylserine liposome treatment was the most efficient and correlated with significantly reduced neuronal death in the retina 7 days after reperfusion. The results of our study indicate that therapeutic strategy based on mimicking a systemic increase in apoptotic signaling can significantly reduce central nervous system damage induced by IR and improve neurologic outcome.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Apoptosis / drug effects*
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Cell Death / drug effects
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Cell Survival / drug effects
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Cytokines / biosynthesis
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Cytokines / immunology
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Disease Models, Animal
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Liposomes
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Male
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Mice
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Mice, Inbred C57BL
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Neurons / drug effects*
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Neurons / immunology
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Neurons / pathology
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Neuroprotective Agents / administration & dosage
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Neuroprotective Agents / pharmacology
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Neuroprotective Agents / therapeutic use*
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Phosphatidylserines / administration & dosage
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Phosphatidylserines / pharmacology
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Phosphatidylserines / therapeutic use*
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Reperfusion Injury / drug therapy*
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Reperfusion Injury / immunology
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Reperfusion Injury / pathology
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Retina / drug effects*
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Retina / immunology
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Retina / pathology
Substances
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Cytokines
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Liposomes
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Neuroprotective Agents
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Phosphatidylserines