The steroid hormone 20-hydroxyecdysone upregulates calcium release-activated calcium channel modulator 1 expression to induce apoptosis in the midgut of Helicoverpa armigera

Li, Yongbo; Pei, Xu-Yang; Wang, Di; Chen, Caihua; Cai, Mei-Juan; Wang, Jinxing; Zhao, Xiao‐Fan

doi:10.1016/j.ceca.2017.10.004

Cited by 15 publications

(15 citation statements)

References 57 publications

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“…In insects, programmed cell death is usually induced by ecdysone (25,26,55). In addition, peak ecdysone titer peaks simultaneously with the autophagy-related gene transcription in most insects (24,26,55).…”

Section: Discussionmentioning

confidence: 99%

“…It was recently shown that, in most insects, the transcription levels of ATG5 and associated genes were the highest during metamorphosis (34,35). In addition, similar to ATG5 in mammals, insect ATG5 is cleaved by calpains, inducing apoptosis after autophagy (25,(34)(35)(36). However, the mechanisms underlying the transition between apoptosis and autophagy in ticks, particularly with respect to salivary gland degeneration, remain unclear.…”

Section: Introductionmentioning

confidence: 99%

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ATG5 is instrumental in the transition from autophagy to apoptosis during the degeneration of tick salivary glands

Wang

Zhang

Luo

et al. 2020

Preprint

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Female tick salivary glands undergo rapid degeneration several days post engorgement. This degeneration may be caused by the increased concentration of ecdysone in the hemolymph during the fast feeding period and both autophagy and apoptosis occur. In this work, we first proved ATG and Caspase gene expression peaks during degeneration of the tick salivary glands. We explored the regulatory role of Rhipicephalus haemaphysaloides autophagy related 5 (RhATG5) in the degeneration of tick salivary glands. During the fast feeding phase, RhATG5 was cleaved and both calcium concentration and the transcription of RhCalpains increased in the salivary glands. Recombinant RhATG5 was cleaved by μ-Calpain only in the presence of calcium; the mutant RhATG5191-199Δ was not cleaved. Treatment with 20-hydroxyecdysone (20E) led to programmed cell death in the salivary glands of unfed ticks in vitro, RhATG8-phosphatidylethanolamine (PE) was upregulated in ticks treated with low concentration of 20E. Conversely, RhATG8-PE decreased and RhCaspase-7 increased in ticks treated with a high concentration of 20E and transformed autophagy to apoptosis. High concentrations of 20E led to the cleavage of RhATG5. Calcium concentration and expression of RhCalpains were also upregulated in the tick salivary glands. RNA interference (RNAi) of RhATG5 in vitro inhibited both autophagy and apoptosis of the tick salivary glands. RNAi of RhATG5 in vivo significantly inhibited the normal feeding process. These results demonstrated that high concentrations of 20E led to the cleavage of RhATG5 by increasing the concentration of calcium and stimulated the transition from autophagy to apoptosis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

ATG5 is instrumental in the transition from autophagy to apoptosis during the degeneration of tick salivary glands

Wang

Zhang

Luo

et al. 2020

Preprint

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“…Aggregated-STIM1 moves toward the plasma membrane to interact with orai1 for Ca 2+ entry [57]. In turn, orai1 expression is upregulated by 20E [58]. The high levels of 20E switches autophagy to apoptosis in the H. armigera midgut by increasing the Ca 2+ levels in cells [59], thereby inducing apoptosis [60].…”

Section: The 20e Signaling Cascade Via Gpcrsmentioning

confidence: 99%

G protein-coupled receptors function as cell membrane receptors for the steroid hormone 20-hydroxyecdysone

Zhao

2020

Cell Commun Signal

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G protein-coupled receptors (GPCRs) are cell membrane receptors for various ligands. Recent studies have suggested that GPCRs transmit animal steroid hormone signals. Certain GPCRs have been shown to bind steroid hormones, for example, G protein-coupled estrogen receptor 1 (GPER1) binds estrogen in humans, and Drosophila dopamine/ecdysteroid receptor (DopEcR) binds the molting hormone 20-hydroxyecdysone (20E) in insects. This review summarizes the research progress on GPCRs as animal steroid hormone cell membrane receptors, including the nuclear and cell membrane receptors of steroid hormones in mammals and insects, the 20E signaling cascade via GPCRs, termination of 20E signaling, and the relationship between genomic action and the nongenomic action of 20E. Studies indicate that 20E induces a signal via GPCRs to regulate rapid cellular responses, including rapid Ca2+ release from the endoplasmic reticulum and influx from the extracellular medium, as well as rapid protein phosphorylation and subcellular translocation. 20E via the GPCR/Ca2+/PKC/signaling axis and the GPCR/cAMP/PKA-signaling axis regulates gene transcription by adjusting transcription complex formation and DNA binding activity. GPCRs can bind 20E in the cell membrane and after being isolated, suggesting GPCRs as cell membrane receptors of 20E. This review deepens our understanding of GPCRs as steroid hormone cell membrane receptors and the GPCR-mediated signaling pathway of 20E (20E-GPCR pathway), which will promote further study of steroid hormone signaling via GPCRs, and presents GPCRs as targets to explore new pharmaceutical materials to treat steroid hormone-related diseases or control pest insects. Graphical abstract

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“…Proteomic sequencing indicated that energy-related proteins were downregulated during salivary gland degeneration, but some proteins associated with the degradation of DNA or proteins were up regulated; certain proteins involved in apoptosis or autophagy were also differentially expressed [31]. Thus, similar to some insects, the degradation of tick salivary glands represents programmed cell death mediated by ecdysone [32][33][34][35][36]. There is also a relationship between autophagy and apoptosis during the degeneration of tick salivary glands [37].…”

Section: Introductionmentioning

confidence: 99%

ATG5 is instrumental in the transition from autophagy to apoptosis during the degeneration of tick salivary glands

et al. 2021

View full text Add to dashboard Cite

Female tick salivary glands undergo rapid degeneration several days post engorgement. This degeneration may be caused by the increased concentration of ecdysone in the hemolymph during the fast feeding period and both autophagy and apoptosis occur. In this work, we first proved autophagy-related gene (ATG) and caspase gene expression peaks during degeneration of the tick salivary glands. We explored the regulatory role of Rhipicephalus haemaphysaloides autophagy-related 5 (RhATG5) in the degeneration of tick salivary glands. During the fast feeding phase, RhATG5 was cleaved and both calcium concentration and the transcription of Rhcalpains increased in the salivary glands. Recombinant RhATG5 was cleaved by μ-calpain only in the presence of calcium; the mutant RhATG5191-199Δ was not cleaved. Treatment with 20-hydroxyecdysone (20E) led to programmed cell death in the salivary glands of unfed ticks in vitro, RhATG8-phosphatidylethanolamine (PE) was upregulated in ticks treated with low concentration of 20E. Conversely, RhATG8-PE decreased and Rhcaspase-7 increased in ticks treated with a high concentration of 20E and transformed autophagy to apoptosis. High concentrations of 20E led to the cleavage of RhATG5. Calcium concentration and expression of Rhcalpains were also upregulated in the tick salivary glands. RNA interference (RNAi) of RhATG5 in vitro inhibited both autophagy and apoptosis of the tick salivary glands. RNAi of RhATG5 in vivo significantly inhibited the normal feeding process. These results demonstrated that high concentrations of 20E led to the cleavage of RhATG5 by increasing the concentration of calcium and stimulated the transition from autophagy to apoptosis.

show abstract

The steroid hormone 20-hydroxyecdysone upregulates calcium release-activated calcium channel modulator 1 expression to induce apoptosis in the midgut of Helicoverpa armigera

Cited by 15 publications

References 57 publications

ATG5 is instrumental in the transition from autophagy to apoptosis during the degeneration of tick salivary glands

ATG5 is instrumental in the transition from autophagy to apoptosis during the degeneration of tick salivary glands

G protein-coupled receptors function as cell membrane receptors for the steroid hormone 20-hydroxyecdysone

ATG5 is instrumental in the transition from autophagy to apoptosis during the degeneration of tick salivary glands

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