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High School Poster Expo

High School Poster Expo

E1-b - Mitochondria Trafficking In Axonal Health And Neuroprotection

Saturday, October 11, 2025
10:00 AM - 12:00 PM PDT
Location: Exhibit Hall F, G & H

Introduction: : Chemotherapy is a treatment that uses powerful drugs to kill fast-growing cancer cells, but it can also damage healthy cells, leaving behind long-term damage that can significantly reduce the quality of life. Cancer drugs such as cisplatin (CDDP) and paclitaxel (PTX) can harm sensory neurons. Inside healthy neurons, mitochondria normally travel along axons to deliver energy for nerve signaling and repair. When this transport system fails, the axons lose energy, shrink towards the cell body, and degenerate. This “dying-back” degeneration often begins at the distal ends of axons, leading to pain, nausea, tingling, and weakness.
In our previous study, we found that microtubule-targeting agents (PTX) were more toxic to axons, while CDDP was more toxic to cell bodies. The FDA-approved drug, fluocinolone acetonide (FA), was also found to be neuroprotective against chemotherapy drugs in vitro, restoring anterograde mitochondrial trafficking.
In this study, we focused on tracking and comparing the mitochondrial movement in the proximal and distal axon segments in the microchannels after treatment with CDDP alone versus CDDP combined with FA, using untreated neurons as the control. Rat dorsal root ganglion (DRG) neurons were cultured in a compartmentalized microfluidic system that separates the cell body (proximal) from axons (distal). This method enabled us to measure mitochondrial movement along the microchannels and apply chemotherapy drugs to each compartment, allowing for direct observation of the neuroprotective effects of FA.

Materials and

Methods: : We used a compartmentalized microfluidic system to isolate the cell bodies and axons for focal administration of cancer drugs. The compartmentalized system contains small microchannels that are 10 μm wide, 500 μm long, and 3 μm deep. This keeps the large cell bodies from crossing over, allowing only axons to grow through, thus separating the cell body from the axonal side as shown in Figure 1. DRG neurons were isolated from an embryonic day 15 (E-15) Sprague Dawley rat and cultured on one side of the microfluidic device. They were then left to grow for 5–6 days until the axons extended through to the other side of the microchannels. Mitoview Green dye was obtained from Biotium, USA, and used to stain the somal chamber containing cell bodies before drug treatment for 30 min–1 h. The mitochondria were imaged immediately after dilution of the dye using a Leica DMi8 Thunder Fluorescence microscope, as seen in Figure 3, and then again 24 h after initial imaging. The data was collected using Fiji-ImageJ to measure the mitochondria movement in triplicate samples. Microsoft Office Excel 2024 was then used to compile all measurement data, where average and standard deviation were calculated.

Results, Conclusions, and Discussions:: Our previous study showed a significant decrease in mitochondrial trafficking when treated with the chemotherapy drug Paclitaxel (PTX). However, treating with fluocinolone acetonide (FA) restored mitochondrial numbers and motility, especially in PTX-treated axons. This suggested that FA enhances the anterograde mitochondrial transport, reducing cancer drug-induced mitochondrial damage. Figure 2 shows a comparison between the number of distal and proximal mitochondria between the control, FA only, PTX only, and FA + PTX. The mitochondria decreased in PTX-only treated axons, while FA + PTX showed neuroprotective effects.
Referencing this preliminary data, this study focused on the distal and proximal mitochondrial trafficking along the microchannels with the untreated control, cisplatin (CDDP) only, and FA+CDDP. Similar to the PTX, CDDP showed degeneration and the lack of mitochondria on the distal side, while FA cotreated with CDDP had much healthier axons as well as more mitochondria extended to the distal side. This indicates that FA cotreatment with CDDP enhances mitochondrial movement from the proximal side to the distal through the microchannels, promoting neuroprotection against CDDP-induced nerve degeneration.

Acknowledgements and/or References (Optional): : Acknowledgments:
I would like to thank our primary PhD mentors, Khayzaran Qubbaj and Prashant Adhikari, for guiding us through the field of neural engineering and nerve regeneration research. I am grateful to our Master’s mentor, Ibraheem Elazzouzi, for his guidance and expertise. I also extend our thanks to our undergraduate mentors, Ulrik Guerrero-Balbuena and Andrew Yang, for instructing us on the foundational skills and experimental protocols necessary in the lab. I especially thank Dr. In Hong Yang for his unwavering support and inspiring us to carry out this research opportunity.

References:
Tiwari, A. P., Tristan, L. J. C., Albin, B., & Yang, I. H. (2023). Fluocinolone Acetonide Enhances Anterograde Mitochondria Trafficking and Promotes Neuroprotection against Paclitaxel-Induced Peripheral Neuropathy. ACS Chemical Neuroscience, 14(11), 2208-2216.

Albin, B., Qubbaj, K., Tiwari, A. P., Adhikari, P., & Yang, I. H. (2023). Mitochondrial trafficking as a protective mechanism against chemotherapy drug-induced peripheral neuropathy: Identifying the key site of action. Life Sciences, 334, 122219.