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Selective temporal and regional alterations of Nogo-A and small proline-rich repeat protein 1A (SPRR1A) but not Nogo-66 receptor (NgR) occur following traumatic brain injury in the rat

Marklund, Niklas LU ; Fulp, Carl T ; Shimizu, Saori ; Puri, Rishi ; McMillan, Asenia ; Strittmatter, Stephen M and McIntosh, Tracy K (2006) In Experimental Neurology 197(1). p.70-83
Abstract

Axons show a poor regenerative capacity following traumatic central nervous system (CNS) injury, partly due to the expression of inhibitors of axonal outgrowth, of which Nogo-A is considered the most important. We evaluated the acute expression of Nogo-A, the Nogo-66 receptor (NgR) and the novel small proline-rich repeat protein 1A (SPRR1A, previously undetected in brain), following experimental lateral fluid percussion (FP) brain injury in rats. Immunofluorescence with antibodies against Nogo-A, NgR and SPRR1A was combined with antibodies against the neuronal markers NeuN and microtubule-associated protein (MAP)-2 and the oligodendrocyte marker RIP, while Western blot analysis was performed for Nogo-A and NgR. Brain injury produced a... (More)

Axons show a poor regenerative capacity following traumatic central nervous system (CNS) injury, partly due to the expression of inhibitors of axonal outgrowth, of which Nogo-A is considered the most important. We evaluated the acute expression of Nogo-A, the Nogo-66 receptor (NgR) and the novel small proline-rich repeat protein 1A (SPRR1A, previously undetected in brain), following experimental lateral fluid percussion (FP) brain injury in rats. Immunofluorescence with antibodies against Nogo-A, NgR and SPRR1A was combined with antibodies against the neuronal markers NeuN and microtubule-associated protein (MAP)-2 and the oligodendrocyte marker RIP, while Western blot analysis was performed for Nogo-A and NgR. Brain injury produced a significant increase in Nogo-A expression in injured cortex, ipsilateral external capsule and reticular thalamus from days 1-7 post-injury (P < 0.05) compared to controls. Increased expression of Nogo-A was observed in both RIP- and NeuN positive (+) cells in the ipsilateral cortex, in NeuN (+) cells in the CA3 region of the hippocampus and reticular thalamus and in RIP (+) cells in white matter tracts. Alterations in NgR expression were not observed following traumatic brain injury (TBI). Brain injury increased the extent of SPRR1A expression in the ipsilateral cortex and the CA3 at all post-injury time-points in NeuN (+) cells. The marked increases in Nogo-A and SPRR1A in several important brain regions suggest that although inhibitors of axonal growth may be upregulated, the injured brain is also capable of expressing proteins promoting axonal outgrowth following TBI.

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publication status
published
keywords
Animals, Blotting, Western, Brain, Brain Injuries, Cell Count, Cornified Envelope Proline-Rich Proteins, Densitometry, Functional Laterality, GPI-Linked Proteins, Hippocampus, Immunohistochemistry, Male, Membrane Proteins, Microtubule-Associated Proteins, Myelin Proteins, Oligodendroglia, Rats, Rats, Sprague-Dawley, Receptors, Cell Surface, Thalamus, Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, Non-P.H.S.
in
Experimental Neurology
volume
197
issue
1
pages
14 pages
publisher
Elsevier
external identifiers
  • pmid:16321384
  • scopus:29144468992
ISSN
0014-4886
DOI
10.1016/j.expneurol.2005.08.029
language
English
LU publication?
no
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6ae63851-ad3a-45a4-bd53-ee69d0424e6d
date added to LUP
2016-12-08 12:18:10
date last changed
2021-06-23 01:09:51
@article{6ae63851-ad3a-45a4-bd53-ee69d0424e6d,
  abstract     = {<p>Axons show a poor regenerative capacity following traumatic central nervous system (CNS) injury, partly due to the expression of inhibitors of axonal outgrowth, of which Nogo-A is considered the most important. We evaluated the acute expression of Nogo-A, the Nogo-66 receptor (NgR) and the novel small proline-rich repeat protein 1A (SPRR1A, previously undetected in brain), following experimental lateral fluid percussion (FP) brain injury in rats. Immunofluorescence with antibodies against Nogo-A, NgR and SPRR1A was combined with antibodies against the neuronal markers NeuN and microtubule-associated protein (MAP)-2 and the oligodendrocyte marker RIP, while Western blot analysis was performed for Nogo-A and NgR. Brain injury produced a significant increase in Nogo-A expression in injured cortex, ipsilateral external capsule and reticular thalamus from days 1-7 post-injury (P &lt; 0.05) compared to controls. Increased expression of Nogo-A was observed in both RIP- and NeuN positive (+) cells in the ipsilateral cortex, in NeuN (+) cells in the CA3 region of the hippocampus and reticular thalamus and in RIP (+) cells in white matter tracts. Alterations in NgR expression were not observed following traumatic brain injury (TBI). Brain injury increased the extent of SPRR1A expression in the ipsilateral cortex and the CA3 at all post-injury time-points in NeuN (+) cells. The marked increases in Nogo-A and SPRR1A in several important brain regions suggest that although inhibitors of axonal growth may be upregulated, the injured brain is also capable of expressing proteins promoting axonal outgrowth following TBI.</p>},
  author       = {Marklund, Niklas and Fulp, Carl T and Shimizu, Saori and Puri, Rishi and McMillan, Asenia and Strittmatter, Stephen M and McIntosh, Tracy K},
  issn         = {0014-4886},
  language     = {eng},
  number       = {1},
  pages        = {70--83},
  publisher    = {Elsevier},
  series       = {Experimental Neurology},
  title        = {Selective temporal and regional alterations of Nogo-A and small proline-rich repeat protein 1A (SPRR1A) but not Nogo-66 receptor (NgR) occur following traumatic brain injury in the rat},
  url          = {http://dx.doi.org/10.1016/j.expneurol.2005.08.029},
  doi          = {10.1016/j.expneurol.2005.08.029},
  volume       = {197},
  year         = {2006},
}