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

Li,Tong; Zhang,Peng; Yuan,Bin; Zhao,Dongliang; Chen,Yueqin; Zhang,Xinzhong

doi:10.3892/ijmm.2013.1253

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

Authors:
- Tong Li
- Peng Zhang
- Bin Yuan
- Dongliang Zhao
- Yueqin Chen
- Xinzhong Zhang
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Affiliations: Department of Neurology, First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan 453100, P.R. China, Institute of Inflammation and Immune Disease, Shantou University Medical College, Shantou, Guangdong 515031, P.R. China, Key Laboratory of Gene Engineering of the Ministry of Education, Sun Yat-sen University, Guangzhou, Guangdong 510275, P.R. China
Published online on: January 22, 2013 https://doi.org/10.3892/ijmm.2013.1253
Pages: 660-666

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Abstract

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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