Abstract
Abstract Neutrophils constitutively undergo apoptosis at both normal and inflamed sites: an important process that limits the toxic potential of the neutrophil. However, the signal pathway for neutrophil apoptosis is currently unknown. In this study, we evaluated the role of p38-mitogen-activated protein kinase (MAPK) in the spontaneous apoptosis of neutrophils in vitro. We found that p38-MAPK was constitutively tyrosine phosphorylated and activated during spontaneous apoptosis of neutrophils. Inhibition of p38-MAPK by SB203580 and an antisense oligonucleotide delayed apoptosis by approximately 24 h. The antioxidants catalase and N-acetylcysteine delayed neutrophil apoptosis, but failed to inhibit phosphorylation and activation of p38-MAPK. Granulocyte-macrophage CSF and anti-Fas Ab, which altered the rate of apoptosis, did not affect phosphorylation and activation of p38-MAPK. These results suggest that the constitutive phosphorylation and activation of p38-MAPK are involved in the program of spontaneous apoptosis in neutrophils.
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Dates
Type | When |
---|---|
Created | 2 years, 8 months ago (Dec. 31, 2022, 9:50 a.m.) |
Deposited | 8 months ago (Jan. 2, 2025, 12:41 p.m.) |
Indexed | 3 months, 2 weeks ago (May 20, 2025, 2:04 p.m.) |
Issued | 26 years, 7 months ago (Feb. 1, 1999) |
Published | 26 years, 7 months ago (Feb. 1, 1999) |
Published Print | 26 years, 7 months ago (Feb. 1, 1999) |
@article{Aoshiba_1999, title={Role of p38-Mitogen-Activated Protein Kinase in Spontaneous Apoptosis of Human Neutrophils}, volume={162}, ISSN={1550-6606}, url={http://dx.doi.org/10.4049/jimmunol.162.3.1692}, DOI={10.4049/jimmunol.162.3.1692}, number={3}, journal={The Journal of Immunology}, publisher={Oxford University Press (OUP)}, author={Aoshiba, Kazutetsu and Yasui, Shuji and Hayashi, Mitsutoshi and Tamaoki, Jun and Nagai, Atsushi}, year={1999}, month=feb, pages={1692–1700} }