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Prostaglandin A2 induces apoptosis in three cell lines derived from the fall armyworm, Spodoptera frugiperda

Yong Wang, Cynthia L. Goodman, Joseph Ringbauer Jr., Yaofa Li, David Stanley
Archives of insect biochemistry and physiology 2021 v.108 no.3 pp. e21844
Spodoptera frugiperda, apoptosis, caspase-1, caspase-2, caspase-3, caspase-5, cell lines, central nervous system, fat body, insects, messenger RNA, prostaglandins
Animals maintain homeostasis of cell numbers, constantly creating new cells and eliminating others. Programmed cell death, apoptosis, is a mechanism of cell elimination and it acts in many aspects of animal biology. Drawing on the biomedical background, several signals launch the apoptosis mechanisms, including prostaglandins (PGs). Based on this information, we posed the hypothesis that PGs similarly induce apoptosis in insect cell lines. We used three Spodoptera frugiperda cell lines, including two newly established, BCIRL‐SfNS‐0518B‐YL derived from the central nervous system and BCIRL‐Sf4FB‐0614‐SGS derived from fat body, and the commercially available Sf9 cells. Using a kinetic apoptosis kit, we found treating SfNS cells for 18 h with 15 or 20 μM PGA₂ led to decreases in cell numbers, coupled with increased numbers of apoptotic and dead cells. Similar exposures to 10 μM PGA₂ (24 h) led to substantial increases in apoptotic cells, confirmed by a terminal deoxynucleotidyl transferase dUTP nick end labeling assay on a flow cytometer. The influence of PGA₂ treatments increased with dosage, as we recorded about 20% apoptosis at 24 h post‐PGA₂ treatments (10 μM) and about 34% apoptosis at 24 h post‐30 μM treatments. PGA₂ treatments led to 10‐ to 30‐fold increases in messenger RNAs (mRNAs) encoding apoptosis‐specific caspases‐1, −2, −3, and −5 at 12 h and 40‐ to 60‐fold increases in mRNAs encoding caspases‐1 and −2, 10‐fold increases for caspases‐3 and −5 at 24 h. These findings strongly support our hypothesis that PGs induce apoptosis in an insect cell line and confirm an additional PG action in insect biology.