Volume 23, No 2, Feb 2013
ISSN: 1001-0602
EISSN: 1748-7838 2018
impact factor 17.848*
(Clarivate Analytics, 2019)
Volume 23 Issue 2, February 2013: 290-299
ORIGINAL ARTICLES
Cytokinin signaling regulates pavement cell morphogenesis in Arabidopsis
Hongjiang Li1,2,3,4, Tongda Xu1,5, Deshu Lin1,6, Mingzhang Wen1, Mingtang Xie1, Jérôme Duclercq3,4, Agnieszka Bielach3,4, Jungmook Kim7, G Venugopala Reddy1, Jianru Zuo8, Eva Benková3,4, Jiří Friml3,4, Hongwei Guo2 and Zhenbiao Yang1
1Center for Plant Cell Biology, Department of Botany and Plant Sciences, University of California, Riverside, CA 92521, USA
2State Key Laboratory of Protein and Plant Gene Research, College of Life Sciences, Peking University, Beijing 100871, China
3Department of Plant Systems Biology, VIB, Technologiepark 927, B-9052 Gent, Belgium
4Department of Plant Biotechnology and Bioinformatics, Ghent University, Technologiepark 927, Gent B-9052, Belgium
5Temasek Life Sciences Laboratory, 1 Research Link, National University of Singapore, Singapore 117604, Singapore
6State Key Laboratory of Plant Physiology and Biochemistry, Department of Plant Sciences, College of Biological Sciences, China Agricultural University, Beijing 100193, China
7Department of Bioenergy Science and Technology, Chonnam National University, Buk-Gu, Gwangju 500-757, South Korea
8State Key Laboratory of Plant Genomics and National Plant Gene Research Center, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China
Correspondence: Bing Sun, Guangxun Meng, Chang Chen,(bsun@sibs.ac.cn; gxmeng@sibs.ac.cn; changchen@moon.ibp.ac.cn)
Inflammasomes are multi-protein complexes that trigger the activation of caspase-1 and the maturation of interleukin-1β (IL-1β), yet the regulation of these complexes remains poorly characterized. Here we show that nitric oxide (NO) inhibited the NLRP3-mediated ASC pyroptosome formation, caspase-1 activation and IL-1β secretion in myeloid cells from both mice and humans. Meanwhile, endogenous NO derived from iNOS (inducible form of NO synthase) also negatively regulated NLRP3 inflammasome activation. Depletion of iNOS resulted in increased accumulation of dysfunctional mitochondria in response to LPS and ATP, which was responsible for the increased IL-1β production and caspase-1 activation. iNOS deficiency or pharmacological inhibition of NO production enhanced NLRP3-dependent cytokine production in vivo, thus increasing mortality from LPS-induced sepsis in mice, which was prevented by NLRP3 deficiency. Our results thus identify NO as a critical negative regulator of the NLRP3 inflammasome via the stabilization of mitochondria. This study has important implications for the design of new strategies to control NLRP3-related diseases.
Cell Research (2013) 23:201–212; doi:10.1038/cr.2013.6; published online 15 January 2013
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