100 Section - Neuroprotection and Functional Recovery in Spinal Cord Injury via clMagR-Expressing Mesenchymal Stem Cells to Alleviate Ferroptosis

Wednesday, May 20, 2026

6:00 PM - 7:30 PM PT

Presenting Author/Autor expositor(s)

LZ

Lijuan Zong, PhD

Ph.D. candidate
Southeast University
Nanjing, Jiangsu, China (People's Republic)

Corresponding Author/Autor a quien dirigir la corr(s)

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hongxing wang, PhD

Professor
Southeast University
Nanjing, Jiangsu, China (People's Republic)

Objectives : Mesenchymal stem cell (MSC) transplantation for spinal cord injury (SCI) has been widely studied, but low graft survival remains a major limitation. Studies have shown that iron overload during the acute phase of injury triggers ferroptosis. Previous work demonstrated that bone marrow-derived MSCs expressing the iron-based magnetosensor (clMagR) can convert extracellular free iron ions into iron oxide nanoparticles. This study aimed to investigate whether clMagR-overexpressing human umbilical cord MSCs (clMagR-hUC-MSCs) could chelate excess iron ions, enhance graft survival during the acute phase of SCI, and promote functional recovery.

Design: Lentiviral transduction was used to overexpress clMagR in hUC-MSCs. SCI rat models were treated with clMagR-hUC-MSC transplantation combined with repetitive transcranial magnetic stimulation (rTMS). Motor function was assessed using BBB scores and electromyography. The viability of clMagR-hUC-MSCs under high-iron conditions and their neuroprotective effects in co-culture systems were evaluated using CCK-8, flow cytometry, Western blot, and immunofluorescence.

Results: The transplantation of clMagR-hUC-MSCs significantly improved BBB scores, gait analysis, and motor-evoked potentials in rats. Immunofluorescence revealed that clMagR-hUC-MSCs persisted longer in the spinal cord compared to hUC-MSCs. In vitro experiments showed that clMagR-hUC-MSCs exhibited enhanced viability under high-iron conditions, with reduced Acsl4 and MDA levels, improved mitochondrial function, and increased neuronal survival in co-culture systems. Flow cytometry confirmed that clMagR-hUC-MSCs restored mitochondrial membrane potential and reduced reactive oxygen species (ROS) accumulation in neurons.

Conclusion:

The transplantation of clMagR into hUC-MSCs prolongs their retention in the spinal cord, mitigates iron overload-induced neuronal damage, and provides neuroprotection, thereby promoting functional recovery after SCI.