Nitric oxide: promoter or suppressor of programmed cell death?
10.1007/s13238-010-0018-x
- Author:
Yiqin WANG
1
;
Chen CHEN
;
Gary J LOAKE
;
Chengcai CHU
Author Information
1. National Key Laboratory of Plant Genomics and National Centre for Plant Gene Research, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Apoptosis;
physiology;
Caspases;
metabolism;
Caspases, Effector;
metabolism;
Cyclic GMP;
metabolism;
Mitochondria;
metabolism;
physiology;
Nitric Oxide;
metabolism;
physiology;
Plant Cells;
Plant Physiological Phenomena;
Signal Transduction;
physiology
- From:
Protein & Cell
2010;1(2):133-142
- CountryChina
- Language:English
-
Abstract:
Nitric oxide (NO) is a short-lived gaseous free radical that predominantly functions as a messenger and effector molecule. It affects a variety of physiological processes, including programmed cell death (PCD) through cyclic guanosine monophosphate (cGMP)-dependent and - independent pathways. In this field, dominant discoveries are the diverse apoptosis networks in mammalian cells, which involve signals primarily via death receptors (extrinsic pathway) or the mitochondria (intrinsic pathway) that recruit caspases as effector molecules. In plants, PCD shares some similarities with animal cells, but NO is involved in PCD induction via interacting with pathways of phytohormones. NO has both promoting and suppressing effects on cell death, depending on a variety of factors, such as cell type, cellular redox status, and the flux and dose of local NO. In this article, we focus on how NO regulates the apoptotic signal cascade through protein S-nitrosylation and review the recent progress on mechanisms of PCD in both mammalian and plant cells.
