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Published on: July 17, 2016
Plasmalogens ensure the stability of non-neuronal (microglial) cells during long-term cytotoxicity
Fatma Ali1, Md Shamim Hossain2, Ahmed Abdeen3,4
1Physiology Department, Faculty of Veterinary Medicine, Aswan University, Aswan, 81528, Egypt.
Abstract:
Microglia (MG) are resident phagocytes in the brain responsible for neuronal maintenance. The regulation of MG necroptosis is required for protecting neurons during neurodegenerative diseases. Therefore, this study proposed to elucidate the molecular mechanisms underlying microglia necroptosis during long-time apoptotic stimuli (lipopolysaccharide, LPS). The protective role of plasmalogens (PLS) was also investigated against LPS insult in MG cells (including BV2 and MG6 cell lines). LPS produced time-dependent decreases in the survival of BV2 and MG6 cells mediated by the caspase signaling pathway. Interestingly, MG death was mediated by caspase-8 and 9 signaling pathways suggesting that MG necroptosis was actively attributed to long-time LPS treatment through intrinsic and extrinsic pathways. Notably, caspase signaling was markedly inhibited in the PLS-pretreated cells; thereby, PLS were capable of maintaining the MG cell population and inhibit the MG necroptosis against the longtime of LPS administration via its antioxidant and anti-inflammatory properties.
Insights
Plasmalogens (PLS) protect brain microglia from death induced by long-term lipopolysaccharide (LPS) exposure. PLS inhibit microglia necroptosis via antioxidant and anti-inflammatory actions, preserving neuronal health.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Microglia (MG) are crucial brain phagocytes for neuronal maintenance.
- Regulating MG necroptosis is vital for neuroprotection in neurodegenerative diseases.
Purpose of the Study:
- Elucidate molecular mechanisms of microglia necroptosis under prolonged lipopolysaccharide (LPS) stimulation.
- Investigate the protective effects of plasmalogens (PLS) against LPS-induced insult in microglia.
Main Methods:
- Utilized BV2 and MG6 cell lines for in vitro studies.
- Administered lipopolysaccharide (LPS) as a time-dependent apoptotic stimulus.
- Assessed cell survival and caspase signaling pathways.
Main Results:
- LPS exposure caused time-dependent decreases in BV2 and MG6 cell survival.
- Microglia death was mediated by caspase-8 and caspase-9 signaling, indicating necroptosis via intrinsic and extrinsic pathways.
- Plasmalogens (PLS) pretreatment significantly inhibited caspase signaling, preserving microglia populations.
Conclusions:
- Long-term LPS treatment induces microglia necroptosis through intrinsic and extrinsic caspase pathways.
- Plasmalogens (PLS) protect microglia against LPS-induced necroptosis.
- PLS exert protective effects through antioxidant and anti-inflammatory mechanisms, maintaining microglia viability.
