Proteinase 3 induces oxidative stress-mediated neuronal death in rat primary cortical neuron
- Authors
- Kwon, Kyoung Ja; Cho, Kyu Suk; Kim, Jung Nam; Kim, Min Kyeong; Lee, Eun Joo; Kim, Soo Young; Jeon, Se Jin; Kim, Ki Chan; Han, Jeong Eun; Kang, Young Sun; Kim, Soohyun; Kim, Hahn Young; Han, Seol-Heui; Bahn, Geonho; Choi, Ji Woong; Shin, Chan Young
- Issue Date
- 26-Aug-2013
- Publisher
- ELSEVIER IRELAND LTD
- Keywords
- Neutrophil; Proteinase 3; Neuron; ROS; Apoptosis
- Citation
- NEUROSCIENCE LETTERS, v.548, pp.67 - 72
- Journal Title
- NEUROSCIENCE LETTERS
- Volume
- 548
- Start Page
- 67
- End Page
- 72
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/14370
- DOI
- 10.1016/j.neulet.2013.05.060
- ISSN
- 0304-3940
- Abstract
- The recruitment of neutrophils into the cerebral microcirculation occurs, especially, in acute brain diseases like a focal cerebral ischemia and plays important role in pathological processes. Proteinase 3 is one of the three major proteinases expressed in neutrophils but no reports are available whether proteinase 3 can modulate neuronal survival. In this study, treatment of cultured rat primary cortical neuron with proteinase 3 induced overt reactive oxygen species production and decreased total glutathione contents as well as disruption of mitochondrial transmembrane potential. Proteinase 3 induced neuronal cell death as evidenced by MTT analysis as well as propidium iodide staining, which was prevented by pretreatment with an antioxidant, N-acetyl cysteine. Proteinase 3 increased activation of procaspase-3 and altered expression level of apoptotic regulator proteins, such as Bcl-2, Bax, and Bcl-xL. Similar to in vitro data, a direct microinjection of proteinase 3 into striatum of rat brain induced neuronal death, which was mediated by reactive oxygen species. These results suggest that proteinase 3 is new essential regulator of neuronal cell death pathway in a condition of excess neutrophil encounter in neuroinflammatory conditions. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
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