Extracellular traps (ETs), primarily composed of DNA and antibacterial peptides, are mainly secreted by neutrophils to inhibit pathogen spread and eliminate microorganisms. Recent reports suggest that microglia can also secrete ETs, and these microglial ETs are associated with various neurological conditions, including nerve injury, tumor microenvironment, and ischemic stroke. However, the components and functions of microglial ETs remain underexplored. Secretagogin (Scgn), a calcium-sensor protein, plays a crucial role in the release of peptide hormones, such as insulin, in endocrine cells; however, its function in immune cells, including microglia, is not well understood. Our study demonstrated that Scgn deficiency can lead to the formation of abnormal ETs. We hypothesized that this may involve the c-Jun N-terminal kinase-myeloperoxidase pathway and autophagy.

Introduction
Materials and Methods
    1. Plasmid construction
    2. Cell culture and generation of secretagogindeficientcells
    3. Immunofluorescence
    4. Protein preparation and immunoblot analysis
    5. Reactive oxygen species detection
    6. NADP+/NADPH measurement
    7. Detection of the extracellular trap
    8. Statistical analysis
Results
    1. Secretagogin is expressed in microglia
    2. Extracellular traps are formed by secretagogindeficiency without external stimuli
    3. Secretagogin silencing does not increase oxidativestress in BV-2 microglia
    4. JNK-MPO pathway and autophagy may contributeto extracellular traps formation in secretagogindeficientmicroglia
Discussion
Funding
Conflicts of Interest
References

• Yu Gyung Kim(Department of Pharmacology, School of Dentistry, Kyungpook National University, Daegu 41940, Republic of Korea)
• Do-Yeon Kim(Department of Pharmacology, School of Dentistry, Kyungpook National University, Daegu 41940, Republic of Korea) Corresponding author