UC San Diego

Neuromas are a type of chronic peripheral nerve injury resulting from unsuccessful nerve regeneration. Neuromas contain improperly woven together axons and result in increased pain and sensitivity. In this study, I explored the role of complement proteins and inflammasomes in early neuroma formation using a mouse model. I conducted survival sciatic nerve transection surgeries on mice, severing one sciatic nerve in each mouse. The proximal stump of the transected nerve and the contralateral uninjured nerve of each mouse were harvested at either a one- or two-week timepoint. I performed RT-qPCR on the proximal injured stumps and the contralateral uninjured nerves. I present data indicating a significant increase in the presence of inflammasome markers ASC and NLRP3 and complement protein C1qB in the injured compared to the control nerves of mice in the two-week timepoint. We also present preliminary findings that suggest an increase in the presence of C1qB, ASC and NLRP3 from the one- to the two- week timepoints. These findings pave the way for a clearer understanding of how the complement system and inflammasomes affect neuroma progression and whether they could be a target for clinical interventions in the future.