The extracellular release of mitochondria in the context of mitophagy in LPS-induced inflammation
Abstract/Contents
- Abstract
- Cellular health is particularly dependent on mitochondrial dynamics and function. Mitochondria have emerged as having a large role in proinflammatory signaling, and similarly, proinflammatory agents seem to affect mitochondrial quality and function. Consequently, inflammation and mitochondrial dysfunction are drivers of many degenerative and acute diseases. Furthermore, dysfunctional, extracellular mitochondria appear to be a signaling agent of inflammation. This begs the exploration of interplay of mitophagy, as a regulator of mitochondrial content and quality, and extracellular mitochondria content in the context of inflammation. Using a RAW 264.7 monocyte/macrophage-like cell line, we characterize changes in mitochondrial function, oxidative stress, autophagy, and intracellular and extracellular mitochondria content in a model of lipopolysaccharide (LPS)-induced inflammation. Here we hypothesized that LPS-induced inflammation in RAW 264.7 cells would result in an increase of extracellular mitochondria, which propagate inflammation, due to stalled mitophagy. We found that LPS reduced mitochondrial respiration and increased mitochondrial reactive oxygen species (ROS) which indeed suggests a role for extracellular mitochondria in propagating inflammation. Furthermore, we found LPS increased both intracellular and extracellular mitochondrial content as shown by FACS analysis which confirms the former part of our hypothesis. However, this was accompanied by the finding of increased autophagic vesicles detected via western blot following treatment with LPS which suggests early-stage autophagy induction. The primary results of this study suggest that LPS-induced inflammation disrupts mitochondrial function and increases extracellular mitochondria despite early-stage autophagy induction.
Description
| Type of resource | text |
|---|---|
| Date modified | May 13, 2022; December 5, 2022 |
| Publication date | May 6, 2022; May 2022 |
Creators/Contributors
| Author | Tsegay, Kaleb |
|---|---|
| Data contributor | Mukherjee, Riddhita |
| Thesis advisor | Vijayan, Vijith |
| Thesis advisor | Haileselassie, Bereketeab |
| Thesis advisor | Mochly-Rosen, Daria |
| Thesis advisor | Shen, Kang |
| Degree granting institution | Stanford University, Department of Biology |
Subjects
| Subject | Cell Biology |
|---|---|
| Subject | Mitophagy |
| Subject | Autophagy |
| Subject | Autophagic vacuoles |
| Subject | Inflammation |
| Subject | Mitochondria |
| Subject | Oxidative stress |
| Genre | Text |
| Genre | Thesis |
Bibliographic information
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- Use and reproduction
- User agrees that, where applicable, content will not be used to identify or to otherwise infringe the privacy or confidentiality rights of individuals. Content distributed via the Stanford Digital Repository may be subject to additional license and use restrictions applied by the depositor.
- License
- This work is licensed under a Creative Commons Attribution Non Commercial 4.0 International license (CC BY-NC).
Preferred citation
- Preferred citation
- Tsegay, K., Mukherjee, R., Vijayan, V., Haileselassie, B., and Mochly-Rosen, D. (2022). The extracellular release of mitochondria in the context of mitophagy in LPS-induced inflammation. Stanford Digital Repository. Available at https://purl.stanford.edu/vs255xr7496
Collection
Undergraduate Theses, Department of Biology, 2021-2022
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- kbtsegay@stanford.edu
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