Major

Chemistry

Anticipated Graduation Year

2023

Access Type

Restricted Access

Abstract

Tumor necrosis factor alpha (TNFɑ) is a proinflammatory cytokine that produces inflammation in airway diseases. TNFɑ increases mitochondrial volume density and O2 consumption rate (OCR) in human airway smooth muscle (hASM) cells; however, when normalized for mitochondrial volume density, the OCR per mitochondrion decreases. Our quantitative histochemical technique measures the maximum velocity of the succinate dehydrogenase reaction (SDHmax) in individual hASM cells. We hypothesized that TNFɑ decreases SDHmax per mitochondrion in individual hASM cells. Following TNFɑ treatment, mitochondrial volume density increases, consistent with reduced SDHmax, suggesting increased ATP demand from TNFɑ is met with increased mitochondrial volume density and SDHmax.

Community Partners

Mayo Clinic

Supported By

Gary Sieck, Ph.D., Mayo Clinic; Sanjana Mahadev Bhat, Ph.D., Mayo Clinic

Comments

This work was completed at Mayo Clinic, Rochester through the Summer Undergraduate Research Fellowship. Thank you to Dr. Gary Sieck, the Regenerative Sciences SURF Team, Dr. Mahadev Bhat, and all those who mentored me during this project.

Creative Commons License

Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License.

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TNFɑ Reduces the Maximum Respiratory Capacity of Mitochondria in hASM Cells

Tumor necrosis factor alpha (TNFɑ) is a proinflammatory cytokine that produces inflammation in airway diseases. TNFɑ increases mitochondrial volume density and O2 consumption rate (OCR) in human airway smooth muscle (hASM) cells; however, when normalized for mitochondrial volume density, the OCR per mitochondrion decreases. Our quantitative histochemical technique measures the maximum velocity of the succinate dehydrogenase reaction (SDHmax) in individual hASM cells. We hypothesized that TNFɑ decreases SDHmax per mitochondrion in individual hASM cells. Following TNFɑ treatment, mitochondrial volume density increases, consistent with reduced SDHmax, suggesting increased ATP demand from TNFɑ is met with increased mitochondrial volume density and SDHmax.