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Int. J. Mol. Sci. 2014, 15(2), 3299-3318;

Expression of PHB2 in Rat Brain Cortex Following Traumatic Brain Injury

The Center Laboratory of Huai'an First People's Hospital Nanjing Medical University, Huai'an 223300, China
Jiangsu Province Key Laboratory of Neuroregeneration, Nantong University, Nantong 226001, China
Affiliated Hospital of Nantong University, Nantong 226001, China
These authors contributed equally to this work.
Author to whom correspondence should be addressed.
Received: 13 November 2013 / Revised: 31 January 2014 / Accepted: 13 February 2014 / Published: 21 February 2014
(This article belongs to the Special Issue Neuroprotective Strategies 2014)
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Prohibitin2 (PHB2) is a ubiquitous, evolutionarily strongly conserved protein. It is one of the components of the prohibitin complex, which comprises two highly homologous subunits, PHB1 and PHB2. PHB2 is present in various cellular compartments including the nucleus and mitochondria. Recent studies have identified PHB2 as a multifunctional protein that controls cell proliferation, apoptosis, cristae morphogenesis and the functional integrity of mitochondria. However its distribution and function in the central nervous system (CNS) are not well understood. In this study, we examined PHB2 expression and cellular localization in rats after acute traumatic brain injury (TBI). Western Blot analysis showed PHB2 level was significantly enhanced at five days after injury compared to control, and then declined during the following days. The protein expression of PHB2 was further analyzed by immunohistochemistry. In comparison to contralateral cerebral cortex, we observed a highly significant accumulation of PHB2 at the ipsilateral brain. Immunofluorescence double-labeling showed that PHB2 was co-expressed with NeuN, GFAP. Besides, PHB2 also colocalized with activated caspase-3 and PCNA. To further investigate the function of PHB2, primary cultured astrocytes and the neuronal cell line PC12 were employed to establish a proliferation model and an apoptosis model, respectively, to simulate the cell activity after TBI to a certain degree. Knocking down PHB2 by siRNA partly increased the apoptosis level of PC12 stimulated by H2O2. While the PHB2 was interrupted by siRNA, the proliferation level of primary cultured astrocytes was inhibited notably than that in the control group. Together with our data, we hypothesized that PHB2 might play an important role in CNS pathophysiology after TBI. View Full-Text
Keywords: traumatic brain injury; Prohibitin2; neuron; astrocyte; proliferation; apoptosis traumatic brain injury; Prohibitin2; neuron; astrocyte; proliferation; apoptosis
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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Xu, T.; Fan, X.; Tan, Y.; Yue, Y.; Chen, W.; Gu, X. Expression of PHB2 in Rat Brain Cortex Following Traumatic Brain Injury. Int. J. Mol. Sci. 2014, 15, 3299-3318.

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