Astrocytic transforming growth factor-beta signaling reduces subacute neuroinflammation after stroke in mice.(Glia 2014, 62(8):1227-40.)

報告日期: 2014/11/07
報告時間: 5:10/6:00
報告學生: 王鐘漢
講評老師: 郭余民
附件下載: 下載[1448-1412238629-1.pdf] 

Astrocytic transforming growth factor-β signaling reduces subacute neuroinflammation after stroke in mice.

Egle Cekanaviciute,Nancy Fathali,Kristian P. Doyle,Aaron M. Williams,

Jullet Han,and Marion S. Buckwalter

 

Glia 2014, 62(8):1227-40.

Speaker:Chung-Han Wang                   Date:2014.11.07

Commentator: Yu-Min Kuo                 Location:Room 602

Abstract

Brain mainly composed by neuron,microglia and astrocyte. When the brain is damaged nerve cells secrete TGFβ that through astrocyte activated TGFβ signal pathway limit neuroinflammation and neuroprotection. Author have previously demonstrated that TGFβ signal to astrocytes, neurons and microglia in the stroke border days after stroke. To investigate whether TGFβ affects astrocyte immunoregulatory function, used transgene mice “Ast-Tbr2DN” where TGFβ signaling is inhibited specifically in astrocytes. Despite having a similar infarct size to wildtype controls, Ast-Tbr2DN mice exhibited significantly more neuroinflammation after distal middle cerebral occlusion (dMCAO) stroke. The peri-infarct cortex of Ast-Tbr2DN mice contained increase activated CD11bmonocytic cells and twice as much immunostaining for the activated microglia and macrophage marker CD68 than controls. Inhibiting Astrocytic TGFβ signaling does not affect initial stroke size or astrocytic activation in the peri-infarct cortex.After dMCAO 2days in Ast-Tbr2DN mice brain unable to upregulate TGF-β1and its activator thrombospondin-1. On photothrombotic motor cortex stroke Ast-Tbr2DN mice have motor dysfunction and bad outcome than control. All data demonstrate here that astrocytic TGFβ signaling functions to limit immune cell infiltration and activation after stroke.

References

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