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.
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.
Hindpaw mechanical withdrawal thresholds and thermal withdrawal latencies were comparable at baseline between PGC-1α+/−
mice. After burn injury, both 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.
Taken together, our data suggest that PGC-1α haploinsufficiency promotes pain chronification after burn injury.