Journal
NEUROSCIENCE LETTERS
Volume 549, Issue -, Pages 168-172Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2013.05.042
Keywords
Interleukin-6; Phosphorylation; Smad3; Spinal cord injury; TGF-beta
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Funding
- Aikeikai, Aichi Medical University, Japan
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Transforming growth factor-beta (TGF-beta) is an anti-inflammatory cytokine and is expressed in the injured spinal cord. TGF-beta signals through receptors to activate Smad proteins, which translocate into the nucleus. In the present study, we investigated the chronological alterations and cellular locations of the TGF-beta/Smad signaling pathway following spinal cord injury (SCI) in mice. ELISA analysis showed that the concentration of interleukin-6 (IL-6) in injured spinal cords significantly increases immediately after SCI, while the concentration of TGF-beta gradually increased after SCI, peaked at 2 days, and then gradually decreased. Immunohistochemical studies revealed that Smad3 was mainly expressed in neurons of the spinal cord. Phosphorylated Smad3 at the C-terminus (p-Smad3C) was stained within the motor neurons in the anterior horn, while phosphorylated Smad3 at the linker regions (p-Smad3L) was expressed in astrocytes within gray matter. These findings suggest that SCI induces gradual increases in TGF-beta and induces different activation of p-Smad3C and p-Smad3L. Phosphorylated Smad3C might be involved in neuronal degeneration after SCI, and p-Smad3L may play a role in glial scar formation by astrocytes. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
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