Understanding How Mechanical Stress Affects Calcium Release in Co-Cultured Neuronal and Smooth Muscle Cells
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open in viewerThe neuromuscular junction serves to connect neurons to muscle fibers allowing for brain signals, that code voluntary and involuntary movement, to be transmitted to muscle fibers that will then contract. This contraction is through calcium. The mechanism for calcium influx in both neuronal and smooth muscle cells is mediated by G-Protein Coupled Receptors (GPCR), that bind the neurotransmitters on the cell membrane and trigger a cascade, eventually releasing intracellular calcium. The goal of this study is to investigate how mechanical stress affects the combined calcium response in neuronal and smooth muscle cells when they are forming a neuromuscular junction model and compare the response of each cell type individually. This is achieved by co-culturing WKO-3M22 smooth muscle cells with PC12 neuronal cells and mechanically stressing them on polydimethylsiloxane polymer dishes. The cell's calcium response was imaged using a fluorescent sensor over time and graphed to view trends. We find that the calcium response increases in the cells forming the neuromuscular junction model when stressed mechanically and stimulated by the neurotransmitter bradykinin. Understanding how the intracellular response of calcium release is affected by formation of the neuromuscular junction, mechanical stress, and neurotransmitter stimulation will further our knowledge of how intracellular calcium response could be affected in an abnormal neuromuscular junction produced by various diseases, as well as the response that might be affected by the action of a drug on GPCRs.
- This report represents the work of one or more WPI undergraduate students submitted to the faculty as evidence of completion of a degree requirement. WPI routinely publishes these reports on its website without editorial or peer review.
- Creator
- Subject
- Publisher
- Identifier
- 65596
- E-project-042822-143521
- Keyword
- Advisor
- Year
- 2022
- Date created
- 2022-04-28
- Resource type
- Major
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