BTEB2 Prevents Neuronal Apoptosis via Promoting Bad Phosphorylation in Rat Intracerebral Hemorrhage Model

Krüppel-like zinc-finger transcription factor 5 (KLF5), known as BTEB2 or IKLF, has several biological functions that involve cell proliferation, development and apoptosis. Previous studies demonstrated that BTEB2 had anti-apoptotic effect in multiple diseases such as esophageal cancer and non-small...

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Bibliographic Details
Published in:Journal of molecular neuroscience 2015-01, Vol.55 (1), p.206-216
Main Authors: Liu, Xiaojuan, Yuan, Damin, Nie, Xiaoke, Shen, Jianhong, Yan, Yaohua, Zhang, Dongmei, Gu, Jianxin
Format: Article
Language:English
Subjects:
Animals
Apoptosis
bcl-Associated Death Protein - metabolism
Biomedical and Life Sciences
Biomedicine
Brain research
Cell Biology
Cell cycle
Cell growth
Cerebral Hemorrhage - metabolism
Hematoma
Hemorrhage
Kinases
Kruppel-Like Transcription Factors - genetics
Kruppel-Like Transcription Factors - metabolism
Laboratory animals
Male
Medical prognosis
Neurochemistry
Neurology
Neurons - metabolism
Neurosciences
PC12 Cells
Phosphorylation
Proteomics
Rats
Rats, Sprague-Dawley
Stroke
Transcription factors
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Summary:Krüppel-like zinc-finger transcription factor 5 (KLF5), known as BTEB2 or IKLF, has several biological functions that involve cell proliferation, development and apoptosis. Previous studies demonstrated that BTEB2 had anti-apoptotic effect in multiple diseases such as esophageal cancer and non-small cell lung cancers (NSCLCs). However, the distribution and function of BTEB2 in CNS diseases remain unknown. In this study, we show that BTEB2 down-regulates neuronal apoptosis during pathophysiological processes of intracerebral hemorrhage (ICH). A rat ICH model was established by behavioral tests. Western blot and immunohistochemistry revealed a remarkable up-regulation of BTEB2 expression surrounding the hematoma after ICH. Double-labeled immunofluorescence showed BTEB2 was mostly co-localized with neurons, rarely with activated astrocytes and microglia. Furthermore, we detected that neuronal apoptosis marker active caspase-3 had co-localizations with BTEB2. In addition, KLF5 knockdown in vitro specifically resulted in increasing neuronal apoptosis coupled with reduced Bad phosphorylation at both ser112 and ser136 residues. All our findings suggested that BTEB2 down-regulated neuronal apoptosis via promoting Bad phosphorylation after ICH.
ISSN:0895-8696
1559-1166
DOI:10.1007/s12031-014-0305-8