Phosphatidylserine-containing liposomes promote maximal survival of retinal neurons after ischemic injury

Galina Dvoriantchikova, Christian Agudelo, Eleut Hernandez, Valery I Shestopalov, Dmitry V Ivanov

Research output: Contribution to journalArticle

25 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)1755-1759
Number of pages5
JournalJournal of Cerebral Blood Flow and Metabolism
Volume29
Issue number11
DOIs
StatePublished - Jul 15 2009

Fingerprint

Retinal Neurons
Phosphatidylserines
Liposomes
Reperfusion
Ischemia
Wounds and Injuries
Phosphatidylcholines
Nervous System
Retina
Therapeutics
Central Nervous System
Inflammation
Gene Expression

Keywords

  • Apoptosis
  • Inflammation
  • Ischemia
  • Liposomes
  • Phosphatidylserine
  • Retinal pathology

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Clinical Neurology
  • Neurology

Cite this

Phosphatidylserine-containing liposomes promote maximal survival of retinal neurons after ischemic injury. / Dvoriantchikova, Galina; Agudelo, Christian; Hernandez, Eleut; Shestopalov, Valery I; Ivanov, Dmitry V.

In: Journal of Cerebral Blood Flow and Metabolism, Vol. 29, No. 11, 15.07.2009, p. 1755-1759.

Research output: Contribution to journalArticle

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