Aβ(1-42) disrupts the expression and function of KLF2 in Alzheimer's disease mediated by p53

Chunyan Wu, Fengling Li, Guosheng Han, Zhihui Liu
Biochemical and Biophysical Research Communications 2013 February 8, 431 (2): 141-5
Alzheimer's disease (AD) is the leading cause of dementia in the elderly. Blood brain barrier (BBB) dysfunction and impaired permeability are implicated in the pathological process of AD, but the underlying mechanisms are poorly understood. Kruppel-like factor 2 (KLF2) plays a critical role in regulating vascular functions, including vascular barrier permeability. The expression patterns and functions of KLF2 in AD progress are still unknown. In the current study, we investigated whether alterations in KLF2 contribute to cerebrovascular dysfunction in AD. Our results demonstrated that decreased expression level of KLF2 in the brains of Tg2576 transgenic mice was due to accumulation of Aβ. Importantly, overexpression of KLF2 could completely rescue impaired expression of tight junction protein Occludin induced by Aβ(1-42) in primary human brain endothelial cells (HBMECs). At last, p53 was verified to mediate Aβ(1-42) induced reduction of KLF2. Overall, this is the first time to report that KLF2 is involved in cerebrovascular dysfunction in Alzheimer's disease.

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