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

Authors: Liu, N  Han, S  Lu, PH  Xu, XM 
Citation: Liu N, etal., J Neurosci Res. 2004 Aug 1;77(3):391-401.
Pubmed: (View Article at PubMed) PMID:15248295
DOI: Full-text: DOI:10.1002/jnr.20167

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) (PLA(2)), 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.


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CRRD Object Information
CRRD ID: 10053688
Created: 2015-07-20
Species: All species
Last Modified: 2015-07-20
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.