Autophagic induction by graphene oxide and its reductives in pulmonary epithelial cells
- Authors
- Shin, Jong Wook; Park, Chang Seok; Jung, Jae Woo; Choi, Jae Cheol; Kim, Jae Yeol; Park, In Won; Choi, Byoung Whui; Kim, Soo Young; Choi, Kyoung Soon
- Issue Date
- Sep-2013
- Publisher
- EUROPEAN RESPIRATORY SOC JOURNALS LTD
- Keywords
- Environment; Cell biology; Interstitial lung disease
- Citation
- EUROPEAN RESPIRATORY JOURNAL, v.42, no.S57
- Journal Title
- EUROPEAN RESPIRATORY JOURNAL
- Volume
- 42
- Number
- S57
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/73598
- ISSN
- 0903-1936
1399-3003
- Abstract
- Background: The graphene is an carbon allotrope with honeycombing structure of one-atom-thick planar sheets. Due to its unique chemicophysical properties, graphene becomes one of vast utilized material for modern electronic, informative technologies especially for medical device. For the consequence of GO manufacturing, biologic toxicity of GO must be concerned. Thus, we studied the cellular proliferation or cytotoxicity and autophagic phenomenon induced by graphene oxide and its reductives in pulmonary epithelial cells.Materials and Methods: A549 cells were cultured in DMEM(Dulbecco’s Modified Eagle’s Medium) with 10% fetal bovine serum. Graphene oxide(GO), reduced GO(rGO), sodium dodecyl amine GO(SDS-GO) and hydrazine-amine GO(DA-GO). MTT was performed for cell proliferation assay. Western blots were done for expression of LC3B-I/LC3B-II, beclin-1 and mTOR.Results: R-GO, SDS-GO, DA-GO and rGO inhibited the proliferation of A549 cells in 24, 48 hours of treatment with concentration- and time-dependent manner. LC3B-I/LC3B-II ratio showed increasing trends in 5, 50 and 200 μ/ml of 4 each GO and but sometimes returned to control range in 200 μ/ml of rGO. Beclin-I expression showed down-regulatory patterns in GO and SDS-GO but not in DA-GO and rGO. The mTOR expression showed lower levels in GO, DA-GO, SDS-GO than that of control.Conclusion: GO and its derivatives can inhibit proliferation and induce autophagy of pulmonary epithelial cells.Acknowledgement: This research was supported by Mid-career Research Program (2011-0028752) through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology
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Collections - College of Engineering > School of Chemical Engineering and Material Science > 1. Journal Articles
- College of Medicine > College of Medicine > 1. Journal Articles

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