[Non-apoptotic, non-necrotic death of neutrophils induced by EP3 agonist--ONO-AE-248].

Abstract

AIM:

To investigate the effect of EP(3) agonist--ONO-AE-248 on neutrophils.

METHODS:

Electron microscopy, MTS assay, RT-PCR and FACS were used to observe the morphology, viability, EP(3) receptor expression and apoptosis of neutrophils treated with ONO-AE-248.

RESULTS:

EP(3) receptor was expressed on neutrophils. ONO-AE-248 rapidly caused a unique form of neutrophil death, showing morphological changes of nucleus, including fusion of the lobules, blebbing and rupture of the nuclear membrane, which were different from typical morphological changes of apoptosis and necrosis. The death was dependent on ATP.

CONCLUSION:

The death of neutrophils caused by ONO-AE-248 is likely to be one of the forms of "non-apoptotic programmed cell death".

• Authors: Jia-jia Liu, Zi Zhang, Hao He, Xin Li, Yan-zheng He
• Journal: Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology (Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi) Vol. 21 Issue 5 Pg. 541-3 (Sep 2005) ISSN: 1007-8738 [Print] China
• PMID: 16143052 (Publication Type: English Abstract, Journal Article)

Chemical References

• ONO AE 248
• PTGER3 protein, human
• Receptors, Prostaglandin E
• Receptors, Prostaglandin E, EP3 Subtype
• Dinoprostone

Topics

• Apoptosis
• Cell Death (drug effects)
• Cells, Cultured
• Dinoprostone (analogs & derivatives, pharmacology)
• Flow Cytometry
• Humans
• Microscopy, Electron, Transmission
• Necrosis
• Neutrophils (cytology, drug effects)
• Receptors, Prostaglandin E (agonists)
• Receptors, Prostaglandin E, EP3 Subtype
• Reverse Transcriptase Polymerase Chain Reaction