STAT3 signaling after traumatic brain injury

Anthony A. Oliva, Yuan Kang, Juliana Sanchez-Molano, Concepciõn Furones, Coleen M Atkins

Research output: Contribution to journalArticle

50 Citations (Scopus)

Abstract

Astrocytes respond to trauma by stimulating inflammatory signaling. In studies of cerebral ischemia and spinal cord injury, astrocytic signaling is mediated by the cytokine receptor glycoprotein 130 (gp130) and Janus kinase (Jak) which phosphorylates the transcription factor signal transducer and activator of transcription-3 (STAT3). To determine if STAT3 is activated after traumatic brain injury (TBI), adult male Sprague-Dawley rats received moderate parasagittal fluid-percussion brain injury or sham surgery, and then the ipsilateral cortex and hippocampus were analyzed at various post-traumatic time periods for up to 7 days. Western blot analyses indicated that STAT3 phosphorylation significantly increased at 30 min and lasted for 24 h post-TBI. A significant increase in gp130 and Jak2 phosphorylation was also observed. Confocal microscopy revealed that STAT3 was localized primarily within astrocytic nuclei. At 6 and 24 h post-TBI, there was also an increased expression of STAT3 pathway-related genes: suppressor of cytokine signaling 3, nitric oxide synthase 2, colony stimulating factor 2 receptor β, oncostatin M, matrix metalloproteinase 3, cyclin-dependent kinase inhibitor 1A, CCAAT/enhancer-binding protein β, interleukin-2 receptor γ, interleukin-4 receptor α, and α-2-macroglobulin. These results clarify some of the signaling pathways operative in astrocytes after TBI and demonstrate that the gp130-Jak2-STAT3 signaling pathway is activated after TBI in astrocytes.

Original languageEnglish
Pages (from-to)710-720
Number of pages11
JournalJournal of Neurochemistry
Volume120
Issue number5
DOIs
StatePublished - Mar 1 2012

Fingerprint

STAT3 Transcription Factor
Brain
Astrocytes
Glycoproteins
Phosphorylation
Oncostatin M Receptors
Colony-Stimulating Factor Receptors
Oncostatin M
Interleukin-4 Receptors
CCAAT-Enhancer-Binding Proteins
Suppressor Genes
Janus Kinases
Percussion
Matrix Metalloproteinase 3
Macroglobulins
Cytokine Receptors
Cyclin-Dependent Kinases
Confocal microscopy
Interleukin-2 Receptors
Granulocyte-Macrophage Colony-Stimulating Factor

Keywords

  • astrocyte
  • inflammation
  • signal transducer and activation of transcription-3
  • traumatic brain injury

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

Cite this

STAT3 signaling after traumatic brain injury. / Oliva, Anthony A.; Kang, Yuan; Sanchez-Molano, Juliana; Furones, Concepciõn; Atkins, Coleen M.

In: Journal of Neurochemistry, Vol. 120, No. 5, 01.03.2012, p. 710-720.

Research output: Contribution to journalArticle

Oliva, AA, Kang, Y, Sanchez-Molano, J, Furones, C & Atkins, CM 2012, 'STAT3 signaling after traumatic brain injury', Journal of Neurochemistry, vol. 120, no. 5, pp. 710-720. https://doi.org/10.1111/j.1471-4159.2011.07610.x
Oliva, Anthony A. ; Kang, Yuan ; Sanchez-Molano, Juliana ; Furones, Concepciõn ; Atkins, Coleen M. / STAT3 signaling after traumatic brain injury. In: Journal of Neurochemistry. 2012 ; Vol. 120, No. 5. pp. 710-720.
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