Discipline: Biological Sciences
Subcategory: Cell and Molecular Biology
Room: Virginia A
Zoya Anderson - University of Alabama at Birmingham
Co-Author(s): Chris Keys, University of Alabama at Birmingham, Birmingham, AL; Katelynn Corder-Grier, University of Alabama at Birmingham, Birmingham, AL; Lynn Dobrunz, University of Alabama at Birmingham, Birmingham, AL; Melissa Harris, University of Alabama at Birmingham, Birmingham, AL
Stem cells are present in numerous tissues and are known to function in injury repair and lifelong tissue maintenance. During aging and in some disease states, there is often an observed decline in the presence and/or functionality of stem cells in affected tissues. Better understanding of the mechanisms that regulate stem cell decline is necessary for the development of means to inhibit stem cell loss or restore regenerative capacity. Melanocyte stem cells (McSCs) are a somatic stem cell population that are found in the bulge of the hair follicle and give rise to the pigment-producing melanocyte. Melanocytes produce melanins that are deposited into the hair to give visible coloration. An obvious sign of McSC dysregulation is premature hair-graying, thus targeted mutations in mouse models that exhibit acute gray hair are ideal subjects to study the mechanisms of stem cell decline. One such hair-graying mouse model overexpresses endogenous neuropeptide Y (NPY), which is a neuropeptide that has been implicated as a factor in stress resiliency. We hypothesize that the overexpression of endogenous NPY causes premature hair-graying by a depletion of McSCs through an autonomous mechanism. Preliminary data from RT-PCR and RT-qPCR analyses indicate that NPY and one of its receptors, NPY1R, are present in skin and other tissues of our NPY over-expressing model when compared to wild type controls, suggesting that NPY is systemically overexpressed in this model. Preliminary data from immunohistochemistry indicate that NPY-overexpressing mice exhibit a significant depletion of McSCs when compared to wild type mice, suggesting that stem cell loss is the cause of premature hair-graying observed in this mouse model. It is unknown whether NPY acts on McSCs and their progeny in an intrinsic or extrinsic manner. We have seen from immunohistochemistry that NPY is ectopically expressed in McSCs and melanocytes of NPY-overexpressing mice, which suggests that NPY may have an intrinsic mode of action. Our future studies aim to elucidate the mechanisms that modulate the effects of systemic NPY overexpression on McSCs and their progeny. NPY is currently being investigated as a therapeutic for mood disorders such as post-traumatic stress disorder, which establishes the importance of understanding how systemic upregulation of the peptide can affect stem cells and other tissues.
Funder Acknowledgement(s): NSF Alabama LSAMP Bridge to the Doctorate Fellowship; UAB Department of Biology
Faculty Advisor: Melissa Harris, firstname.lastname@example.org
Role: For this project, I maintained the mouse line/colony through breeding; I performed immunohistochemistry on skins of the mice; I performed RT-qPCR on spleens, hearts, and skins of the mice.