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Thrombin-induced TGF-β1 pathway: a cause of communicating hydrocephalus post subarachnoid hemorrhage

Tong Li1, Peng Zhang, Bin Yuan

  • 1Department of Neurology, First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan 453100, PR China.

International Journal of Molecular Medicine
|January 23, 2013
PubMed

The mechanism of communicating hydrocephalus after subarachnoid hemorrhage (SAH) remains unclear. Revealing a signaling cascade may provide significant insights into the molecular etiology of the accumulation of cerebrospinal fluid (CSF) in cerebral compartments during SAH. To investigate the mechanism of the communicating hydrocephalus following SAH, we infused CSF with thrombin (TH), resulting in proinflammatory and proliferative responses in rat meninges of SAH. The effect of TH could be completely blocked by a transforming growth factor β1 (TGF-β1) inhibitor, SB-431542, suggesting that TH-stimulated proliferation of meninges is through the TGF-β1 signaling pathway. The cascade of TGF β1-Smad3 was significantly upregulated by TH, which, in turn, stimulated the proliferation of subarachnoid meninges. TH-induced overexpression of TGF-β1 and activation of its downstream factors might be a mechanism of communicating hydrocephalus after SAH.

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