Sydney Swedick: Proline Restores Age-associated Loss of Mitochondrial Function

Mitochondrial dysfunction has been widely regarded as an aging hallmark, driving cellular dysfunctions and worsening with age.

Final Project Outcome

About the project

Emanuela Gionfriddo, with the department of chemistry, is photographed with students, in her research lab in the Natural Sciences Complex in April 2024.

What I did:

My project will try to extend this to mammalian cells and investigate the effect of proline on mitochondrial function in a cellular senescence model by employing two models of aging: replicative senescence of human Mesenchymal Stem Cells (MSC) and DNA-damage (etoposide) induced senescence model. It has been recently found in the lab through RNA sequencing for the underlying molecular mechanism that the proline biosynthesis pathway was downregulated in aged cells, as well as that the treatment of senescent stem cells with proline restored mitochondrial function after 7 days by inducing mitophagy evidenced by upregulation of the PINK-PARKIN signaling pathway and staining of LC3 and Tomm20 indicating that mitochondria were marked for degradation. In my work I aim to confirm this work previously through RT-PCR, Western Blot, and intracellular proline content, as well as take my own reins on the project by seeking to elucidate the effects of proline after treatment for 14 days.

What I Learned:

Working in Dr. Stelios Andreadis’ Lab opened my eyes to the field of regenerative medicine. I worked on understanding mitochondrial dysfunction in regards to its impact on cellular senescence and aging. I was able to gain a wide range of skills from RT-PCR, Western Blot, to cell culture, along with enhancing my critical thinking skills and professional skills through working in a laboratory environment with the guidance of supportive mentors. This experience solidified my desire to attend graduate school where I will develop a biohybrid device to restore sensory perception after nerve injuries.

 

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