Different modifications of phosphorylated Smad3C and Smad3L through TGF-β after spinal cord injury in mice

Masahiro Joko, Koji Osuka, Nobuteru Usuda, Kimie Atsuzawa, Masahiro Aoyama, Masakazu Takayasu

Research output: Contribution to journalArticlepeer-review

13 Citations (Scopus)


Transforming growth factor-β (TGF-β) is an anti-inflammatory cytokine and is expressed in the injured spinal cord. TGF-β 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-β/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-β 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-β 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.

Original languageEnglish
Pages (from-to)168-172
Number of pages5
JournalNeuroscience Letters
Publication statusPublished - 09-08-2013
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • General Neuroscience


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