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Anesth Analg. 2019 Feb 27. doi: 10.1213/ANE.0000000000004086. [Epub ahead of print]

Proliferator-Activated Receptor-Gamma Coactivator-1α Haploinsufficiency Promotes Pain Chronification After Burn Injury.

Author information

1
From the Department of Anesthesia, Critical Care and Pain Medicine, Center for Translational Pain Research, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.
2
Department of Anesthesiology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
3
Department of Anesthesiology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
4
Department of Anesthesiology, The First Affiliated Hospital of Zhejiang University, Hangzhou, China.
5
Department of Anesthesiology, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China.
6
Institute of Neuroscience and Department of Neurology of the Second Affiliated Hospital of Guangzhou Medical University, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou, China.
7
McGovern Institute for Brain Research at the Massachusetts Institute of Technology, Cambridge, Massachusetts.

Abstract

BACKGROUND:

Tissue injuries such as surgery and trauma are usually accompanied by simultaneous development of acute pain, which typically resolves along with tissue healing. However, in many cases, acute pain does not resolve despite proper tissue repair; rather, it transitions to chronic pain. In this study, we examined whether proliferator-activated receptor-gamma coactivator-1α (PGC-1α), a master regulator of mitochondria biogenesis, is implicated in pain chronification after burn injury in mice.

METHODS:

We used PGC-1α+/+ and littermates PGC-1α+/- mice of both sex. Burn injury was induced on these mice. Hindpaw mechanical withdrawal thresholds and thermal withdrawal latency were examined.

RESULTS:

Hindpaw mechanical withdrawal thresholds and thermal withdrawal latencies were comparable at baseline between PGC-1α+/- and PGC-1α+/+ mice. After burn injury, both PGC-1α+/+ and PGC-1α+/- mice exhibited an initial dramatic decrease of withdrawal parameters at days 3 and 5 after injury. While PGC-1α+/+ mice fully recovered their withdrawal parameters to preinjury levels by days 11-14, PGC-1α+/- mice failed to recover those parameters during the same time frame, regardless of sex. Moreover, we found that PGC-1α+/- mice resolved tissue inflammation in a similar fashion to PGC-1α+/+ mice using a chemiluminescence-based reactive oxygen species imaging technique.

CONCLUSIONS:

Taken together, our data suggest that PGC-1α haploinsufficiency promotes pain chronification after burn injury.

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