Melissa L. Palmer, PhD

Mentor:  Scott O’Grady, PhD

Current Position:   Assistant Professor, College of Biological Sciences, University of Minnesota

T32 Support: 2003 – 2004 (Pre-doctoral Trainee)
                      2005 – 2007 (Post-doctoral Trainee)

Education:     1983 – 1988, B.S., University of Florida, Gainesville, Florida
                      1999 – 2001, M.D., University of Minnesota
                      2001 – 2005, Ph.D., University of Minnesota

Project:          Dr. Palmer’s research focused on a project involving the role of anion secretion in a model epithelial cell line with properties similar to airway gland epithelial cells. Immortalized endometrial gland epithelial (PEG) cells were grown on Transwell membrane filters under serum-free conditions and exhibited basal ENaC-mediated Na⁺ absorption. Apical stimulation with UTP inhibited Na⁺ transport and activated CFTR and CaCC-dependent anion secretion that oscillated over time. Incubation of cells with 20 nM 17?estridiol for 96 hours enhanced the magnitude and frequency of the Isc oscillations elicited by UTP. In contrast, treatment with progesterone (100 nM) significantly reduced the UTP-stimulated Isc and its subsequent oscillations. QRT-PCR analysis revealed that PEG cells express P2Y₂, P2Y₄ and P2Y₆ receptors, with P2Y₂ in greatest abundance. Stimulation with estrogen had no effect on P2Y₂ or P2Y₆ mRNA expression compared to serum-free conditions, but significantly reduced P2Y₄ mRNA by more than 80%. In contrast, progesterone stimulation inhibited both P2Y₄ and P2Y₆ mRNA expression by more than 90%. Additionally, estrogen and progesterone reduced mRNA expression for KCNQ1 and SK4 K⁺ channels present in the basolateral membrane by approximately 65%. However, UTP stimulated the activity of a basolateral K⁺ channel that exhibited current oscillations similar to the oscillations in Isc observed in experiments with the intact epithelium. The results of the experiments demonstrated that estrogen and progesterone differentially regulate the responsiveness of PEG cells to UTP by altering the expression pattern of P2Y receptors that bind the nucleotide and by basolateral K⁺ channels that play a role in sustaining the electrical driving force for anion secretion.

Publications:

Palmer ML, Fahrenkrug SC, O'Grady SM.  RNA interference and ion channel physiology.  Cell Biochem and Biophys 2006; 46(2):175-91.

Palmer ML, SY Lee, D Carlson, SC Fahrenkrug, and SM O'Grady. Stable knockdown of CFTR establishes a role for the channel in P2Y receptor-stimulated anion secretion. J Cell Physiol 2006; 206:759-770.

Palmer ML, SY Lee, PJ Maniak, D Carlson, SC Fahrenkrug, and SM O'Grady. Protease-activated receptor regulation of Cl- secretion in Calu-3 cells requires prostaglandin release and CFTR activation. Am J Physiol [Cell Physiology] 2006; 290:1189-1198.

Lee SY, Palmer ML, Maniak PJ, Jang SH, Ryu PD, O'Grady SM.  P2Y receptor regulation of sodium transport in human mammary epithelial cells.  Am J Physiol 2007; 293(5):C1472-80.

Palmer ML, KR Schiller, SM O'Grady.  Apical SK potassium channels and Ca2+-dependent anion secretion in endometrial epithelial cells.  J Physiol 2008; 586:717-26.

Last updated 3-26-2008