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GRASP55 and UPR Control Interleukin-1β Aggregation and Secretion.
Marioara Chiritoiu1, Nathalie Brouwers1, Gabriele Turacchio2
1Centre for Genomic Regulation (CRG), The Barcelona Institute for Science and Technology, Dr. Aiguader 88, Barcelona 08003, Spain.
Developmental Cell
|March 19, 2019
Summary
GRASP55 and IRE1α are crucial for secreting mature interleukin-1β (mIL-1β). GRASP55 deficiency impairs mIL-1β secretion and unfolded protein response, revealing new roles for these proteins in inflammatory signaling.
Area of Science:
- Cell Biology
- Immunology
- Molecular Biology
Background:
- Interleukin-1β (IL-1β) is a key inflammatory cytokine.
- Mature IL-1β (mIL-1β) secretion occurs independently of the endoplasmic reticulum.
- The mechanisms governing mIL-1β secretion are not fully understood.
Purpose of the Study:
- To investigate the role of GRASP55 in mIL-1β secretion.
- To explore the connection between GRASP55, the unfolded protein response (UPR), and mIL-1β secretion.
Main Methods:
- Utilized GRASP55 knockout (GRASP55-/-) mice macrophages.
- Assessed mIL-1β secretion and intracellular localization.
- Investigated the unfolded protein response (UPR) pathways, specifically IRE1α and PERK.
- Inhibited IRE1α and PERK pathways to determine their effects on mIL-1β.
Main Results:
- GRASP55-/- macrophages exhibited defective mIL-1β secretion, with mIL-1β accumulating intracellularly.
- GRASP55 deficiency was associated with defects in the IRE1α branch of the UPR.
- Inhibition of IRE1α impaired mIL-1β secretion and led to intracellular aggregation.
- PERK inhibition affected caspase-1-mediated conversion of proIL-1β to mIL-1β.
Conclusions:
- GRASP55 is essential for efficient mIL-1β secretion from macrophages.
- GRASP55 and the IRE1α pathway are critical for maintaining mIL-1β in a secretion-competent state.
- PERK and IRE1α exhibit translation-independent functions in regulating IL-1β production and secretion.
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