Graduation Date

Spring 5-4-2019

Document Type

Thesis

Degree Name

Master of Science (MS)

Programs

Medical Anatomy

First Advisor

Dr. Erika Boesen

Abstract

Prostaglandins are paracrine and autocrine signaling molecules that play important roles through various physiological and pathophysiological functions in the human body including the inflammatory response, control of blood pressure, and water and salt homeostasis in the kidney. Prostaglandins have been shown to have great influence on kidney function. In particular, prostaglandin E2 influences the function of the collecting duct, primarily decreasing vasopressin-stimulated collecting duct water permeability. The aim of this study was to see how various treatments to cells, as well as different growth times, impacted prostaglandin production between two different collecting duct cell lines, one arising from the cortical collecting duct and the other arising from the inner medullary collecting duct. This was accomplished by growing and culturing the cells on 6-well plates, collecting the cell media and measuring prostaglandin accumulation via Enzyme-linked immunosorbent assay (ELISA) kits. Results showed that longer growth times decreased prostaglandin E2 and F2α accumulation in both cell lines. The effect of dDAVP, a vasopressin analog, increased prostaglandin accumulation in the inner medullary collecting duct cells, and increased PGF2α while having virtually no effect on PGE2 in the cortical collecting duct cells. The addition of a cyclooxygenase-1 and cyclooxygenase-2 inhibitor significantly decreased prostaglandin accumulation in both cell lines. Finally, changing the osmolarity of the media by adding sodium chloride (NaCl) increased prostaglandin accumulation in both cell lines. Prostaglandin synthesis has relevant clinical implications, as non-steroidal anti-inflammatory drugs, a common over-the-counter group of pain medications, inhibit cyclooxygenase, an enzyme involved in the biosynthesis of prostaglandins.

Available for download on Wednesday, October 23, 2019

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