ArticleFrontiers in cell and developmental biology2024
Impact of endoplasmic reticulum aminopeptidases 1 (ERAP1) and 2 (ERAP2) on neutrophil cellular functions.
Article in Frontiers in cell and developmental biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Review
- Unveiling the impact of ERAP1 and ERAP2 on migration, angiogenesis and ER stress response.Frontiers in cell and developmental biology · 2025Review
- Impact of ERAP1 downregulation on the pathogenesis of DSS-induced colitis and therapeutic response to sulfasalazine.Frontiers in immunology · 2025Article
- Epigenetic, histological and clinical characterization of preeclampsia in oocyte donation pregnancies: insights into immune dysregulation and microRNA-mediated pathways.Frontiers in cell and developmental biology · 2025Article
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Authors and funding
12 authors.
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Abstract
Introduction: Endoplasmic reticulum aminopeptidases 1 (ERAP1) and 2 (ERAP2) modulate a plethora of physiological processes for the maintenance of homeostasis in different cellular subsets at both intra and extracellular level. Materials and methods: In this frame, the extracellular supplementation of recombinant human (rh) ERAP1 and ERAP2 (300 ng/ml) was used to mimic the effect of stressor-induced secretion of ERAPs on neutrophils isolated from 5 healthy subjects. In these cells following 3 h or 24 h rhERAP stimulation by Western Blot, RT-qPCR, Elisa, Confocal microscopy, transwell migration assay, Oxygraphy and Flow Cytometry we assessed: i) rhERAP internalization; ii) activation; iii) migration; iv) oxygen consumption rate; v) reactive oxygen species (ROS) accumulation; granule release; vi) phagocytosis; and vii) autophagy. Results: We observed that following stimulation rhERAPs: i) were internalized by neutrophils; ii) triggered their activation as witnessed by increased percentage of MAC-1 Conclusion: Our study provides novel insights into the biological role of ERAPs, and indicates that extracellular ERAPs, contribute to shaping neutrophil homeostasis by promoting survival and tolerance in response to stress-related inflammation. This information could contribute to a better understanding of the biological bases governing immune responses, and to designing ERAP-based therapeutic protocols to control neutrophil-associated human diseases.
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