ArticleCell death & disease2016
Nitric oxide-mediated apoptosis of neutrophils through caspase-8 and caspase-3-dependent mechanism.
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 119 citations in OpenAlex.
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- Implications of notoginsenoside R1 in osteoclastogenesis and bone remodeling via nitric oxide modulation.BMC complementary medicine and therapies · 2026Article
- Dual roles of immunosenescence in cancer immunotherapy.Frontiers in immunology · 2026Review
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- Respiratory infection with Enterovirus D68 induces severe acute lung inflammation in the pediatric ferret model.iScience · 2025Article
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- Li Qi Huo Xue Di Wan alleviates hypoxia-induced injury in human cardiac microvascular endothelial cells by inhibiting apoptosis and necroptosis pathways.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Article
- Factors Contributing to the High Malignancy Level of Cholangiocarcinoma and Its Epidemiology: Literature Review and Data.Biology · 2025Review
- Semaphorin 7a is protective through immune modulation during acetaminophen-induced liver injury.Journal of inflammation (London, England) · 2025Article
- Inflammation: a matter of immune cell life and death.npj biomedical innovations · 2025Review
- Diosmetin Inhibits NETs Formation in Neutrophils Through Regulating Nrf2 Signaling.Thoracic cancer · 2025Article
- The relationship between biological aging and psoriasis: evidence from three observational studies.Immunity & ageing : I & A · 2025Article
- New insights into constitutive neutrophil death.Cell death discovery · 2025Review
- The roles of neutrophils in cardiovascular diseases.Frontiers in cardiovascular medicine · 2025Review
- The crosstalk between senescence, tumor, and immunity: molecular mechanism and therapeutic opportunities.MedComm · 2025Review
- Immune aging and infectious diseases.Chinese medical journal · 2024Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophils play an indispensable role in killing of invading pathogens by enhancing reactive oxygen species (ROS) and NO generation, and subsequently undergoing apoptosis. Unlike ROS/NOX2, role of NO/NOS still remains undefined in the apoptosis of neutrophils (PMNs) and the present study attempts to decipher the importance of NO/NOS in the neutrophil apoptosis. Prolonged treatment of human PMNs or mice bone marrow derived neutrophils (BMDN) with NO led to enhanced ROS generation, caspase-8/caspase-3 cleavage, reduced mitochondrial membrane potential and finally cellular apoptosis. NO-induced ROS generation led to caspase-8 deglutathionylation and activation, which subsequently activated mitochondrial death pathway via BID (Bcl-2 family protein) cleavage. NO-mediated augmentation of caspase-8 and BID cleavage was significantly prevented in BMDN from neutrophil cytosolic factor-1 (NCF-1) knockout (KO) mice, implying the involvement of NOX2 in NO-induced apoptosis of PMNs. Furthermore, ROS, NO generation and inducible nitric oxide synthase (iNOS) expression were enhanced in a time-dependent manner in human PMNs and mice BMDN undergoing spontaneous apoptosis. Pharmacological and genetic ablation of iNOS in human PMNs and mice BMDN significantly reduced the levels of apoptosis. Impaired apoptosis of BMDN from iNOS KO mice was due to reduced caspase-8 activity which subsequently prevented caspase-3 and -9 activation. Altogether, our results suggest a crucial role of NO/iNOS in neutrophil apoptosis via enhanced ROS generation and caspase-8 mediated activation of mitochondrial death pathway.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.