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A Mouse Model of Orthopedic Surgery to Study Postoperative Cognitive Dysfunction and Tissue Regeneration
Published on: February 27, 2018
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Surgery-induced cognitive dysfunction is alleviated through triggering receptor expressed on myeloid cells 2
Wen Niu1, Lei Ma2, Tianqi Tao3
1Department of Pathophysiology, Institute of Basic Medical Science, PLA General Hospital, Beijing, 100853, China; Department of Physiology and Pathophysiology, The Fourth Military Medical University, Xi'an, 710032, China.
Acta Histochemica
|May 9, 2020
Summary
Surgery impairs learning and memory by reducing triggering receptor expressed on myeloid cells 2 (TREM2). Upregulating TREM2 with HSP60 improved cognitive function and reduced neuroinflammation in mice.
Area of Science:
- Neuroscience
- Immunology
- Surgical Research
Background:
- Neuroinflammation is critical in perioperative neurocognitive disorders (PND).
- Triggering receptor expressed on myeloid cells 2 (TREM2) shows potential in mitigating brain inflammatory responses.
Purpose of the Study:
- To investigate the role of TREM2 in surgery-induced cognitive dysfunction in adult mice.
- To determine if TREM2 modulation can alleviate post-surgical cognitive deficits.
Main Methods:
- Adult C57BL/6 mice underwent intramedullary fixation surgery.
- TREM2 expression was modulated using a selective TREM2 agonist (HSP60) and TREM2-siRNA.
- Cognitive function, neuroinflammation, and neuronal apoptosis were assessed.
Main Results:
- Surgery worsened learning and memory while reducing TREM2 expression.
- HSP60-induced TREM2 upregulation significantly improved cognitive function, reduced neuroinflammation, and decreased neuronal apoptosis.
- TREM2-siRNA reversed the beneficial effects of HSP60.
Conclusions:
- Upregulation of TREM2 alleviates neuroinflammation.
- TREM2 activation improves learning and memory function following surgery in mice.
- Targeting TREM2 may offer a therapeutic strategy for preventing PND.
