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Title of Journal: Apoptosis

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Abbravation: Apoptosis

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Springer US

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DOI

10.1016/0026-2714(73)90114-5

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1573-675X

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Lymphocytederived microparticles induce apoptosis

Authors: Qian Qiu Wei Xiong Chun Yang Xiaotian Dai Xiaoping Dan Zaixing Yang Yan Jiao Yang Xiang Guoxiang Liu Pierre Hardy
Publish Date: 2014/04/29
Volume: 19, Issue: 7, Pages: 1113-1127
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Abstract

The airway epithelium is critical for the normal integrity and function of the respiratory system Excessive epithelial cell apoptosis contributes to cell damage and airway inflammation We previously demonstrated that lymphocytederived microparticles LMPs induce apoptosis of human bronchial epithelial cells However the underlying mechanisms contributing to LMPsevoked epithelial cell death are largely unknown Here we used bronchial and lung tissue cultures to confirm the proapoptotic effects of LMPs In cell culture experiments we found that LMPs induced human airway epithelial cell apoptosis with associated increases in caspase3 activity In addition LMPs treatment triggered oxidative stress in epithelial cells by enhancing production of malondialdehyde superoxide and reactive oxygen species ROS and by inhibiting production of the antioxidant glutathione Moreover decreasing cellular ROS with the antioxidant Nacetylcysteine rescued epithelial cell viability Together these results demonstrate an important role for oxidative stress in LMPsinduced cell death In epithelial cells LMPs treatment induced phosphorylation of p38 MAPK and arachidonic acid accumulation Moreover arachidonic acid was significantly cytotoxic towards LMPstreated epithelial cells whereas inhibition of p38 MAPK was protective against these cytotoxic effects Similarly inhibition of arachidonic acid production led to decreased caspase3 activity thus rescuing airway epithelial cells from LMPsinduced cell death In conclusion our results show that LMPs induce airway epithelial cell apoptosis by activating p38 MAPK signaling and stimulating production of arachidonic acid with consequent increases in oxidative stress and caspase3 activity As such LMPs may be regarded as deleterious markers of epithelial cell damage in respiratory diseasesQian Qiu is a recipient of award from the State Scholarship Fund of the Ministry of Education of Peoples’ Republic of China 20120761002 Department of Respiratory Medicine Southwest Hospital Chongqing China supported this work We thank Dr Qiaonan Guo for helping with histopathological examination Dr Ju Lu for her generous help with scanning electron microscopy Deying Chen for TUNEL assay Fengjun Wang for constructive suggestions Zhi Yang and Dechang Chen for animal experiment and Liang Wang for technical assistance They are all from Third Military Medical University This work is supported by Grants from the Key Science Technology Research Foundation of Chongqing Science Committee China 2010AA5032 from the Foundation of Achievement Translation of Third Military Medical University China 2010XZH09 and from the Canadian Institutes of Health Research 178918

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