Upregulation of annexins I, II, and V after traumatic spinal cord injury in adult rats

Naikui Liu, Shu Han, Pei Hua Lu, Xiao Ming Xu

Research output: Contribution to journalArticle

39 Scopus citations


The posttraumatic inflammatory reaction contributes to progressive tissue damage after spinal cord injury (SCI). Annexins, a family of structurally related calcium- and phospholipid-binding proteins, have potent anti-inflammatory effects by inhibiting the activity of phospholipase A 2 (PLA2), a key enzyme responsible for inflammation and cytotoxicity. We investigated spatiotemporal expression of annexins I, II, and V after a contusive SCI using the New York University impact device (a 10-g rod, height 12.5 mm) in adult rats. Western blot analysis revealed that annexin I expression increased at 3 days after injury, peaked at 7 days (1.75-fold above the baseline level; P < 0.01), started to decline at 14 days, and returned to the baseline level at and beyond 28 days post-injury. The expression of annexin II started to increase at 3 days, reached its maximal level at 14 days (2.73-fold; P < 0.01), remained at a high level up to 28 days, and then declined to the basal level by 56 days after injury. Annexin V expression started at 3 days, reached its maximal level at 7 days (1.61 -fold; P < 0.05) and remained at this level until 56 days after injury. RT-PCR results confirmed expression of all three annexins at the mRNA level after SCI. Immunohistochemistry and immunofluorescence double-labeling analyses revealed that increased annexins I, II, and V were localized in neurons and glial cells. The present study thus revealed increased expression of the three annexin isoforms after moderate contusive SCI. The precise role of annexins in posttraumatic inflammation and neuroprotection after SCI remains to be determined.

Original languageEnglish (US)
Pages (from-to)391-401
Number of pages11
JournalJournal of Neuroscience Research
Issue number3
StatePublished - Aug 1 2004
Externally publishedYes


  • Annexins
  • Inflammation
  • Neuroprotection
  • Spinal cord injury

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience

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