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IUPUI Student Research & Engagement Day Abstract Book IUPUI Student Research & Engagement Day Abstract Book A Effect of Mechanical Loading on Osteoblasts in vitro Sabria A. Abufares1, John Damrath23, Joseph M. Wallace1 1Department of Biomedical Engineering, Purdue School of Engineering & Technology, Indiana University-Purdue University Indianapolis; 2IU School of Medicine; 3Weldon School of Biomedical Engineering Mechanical loading has been shown to stimulate changes within bone structure, often characterized by collagen production and mineralization. A staple when studying bone, mechanical loading is most often done with whole bones on a holistic scale. Comparatively, little is understood on the microscale of the immediate response bone cells have when stimulated by mechanical loading. Cyclic loading causes fatigue in whole bone, accumulating microcracks that can result in catastrophic failure often seen in patients with degenerative bone diseases such as osteoporosis imperfecta (OI). While cyclic loading has the capability to fracture whole bone, it can lead to a formative response by modeling or remodeling the bone tissue. By studying the immediate pathways that are activated by a mechanical load, the knowledge bank on the cellular response can be expanded. Cyclic loading was done on murine bone cells to understand the immediate action that bone cells have in response to mechanical stimulation. In this study the Flexcell 5000 was used, radially stretching the cell substrate to 10% strain for 600 sinusoidal cycles over a 20-minute period and compared to plated but unstretched bone cells. Pronectin-coated 6-well plates were also used to identify how the extracellular matrix may play a role in cellular expression. After cyclic loading, the cell signals were then quantified using q-PCR. The aim for the research project is to understand the degree of the effect mechanical stimulation has on bone cells in vitro, focusing on the expression of collagen production. Mentors: Joseph M. Wallace, Department of Biomedical Engineering, Purdue School of Engineering & Technology, Indiana University- Purdue University Indianapolis LC-MS/MS Detects Urobilinoids from Feces in Fly Guts Lyunade Adebowale1, Christine Skaggs1, Charity Owings2, Christine Picard2and Nick Manicke11Department of Chemistry, Indiana University-Purdue University Indianapolis; 2Department of Biology, Indiana University-Purdue University Indianapolis. Blow flies are suspected to carry pathogens from one location to another due to the consumption of fecal matter leading to the contamination of food sources. Gut extracts of the blow flies were prepared and then analyzed to detect various tetrapyrrole urobilinoids, commonly found in fecal matter, using liquid chromatography-mass spectrometry. The flies analyzed were from three feeding treatments: unfed flies, liver fed flies, and feces fed flies. Confirmatory tests were run on fly extracts where different types of animal feces were consumed to verify that the urobilinoid compounds would be present regardless of the type of fecal matter consumed (omnivore, herbivore, carnivore). The blow flies were analyzed using a Thermo LTQ-XL mass spectrometer (San Jose, CA) coupled to an Agilent 1100 HPLC (Santa Clara, CA). We used reversed phase chromatography on a 100 x 2.1 mm C18 column at a flow rate of 200 uL/min to separate the urobilinoids of interest. The solvents used were 0.1% formic acid in water (solvent A) and 0.1% formic acid in 70:30 acetonitrile:methanol (solvent B). The data were acquired in positive ion mode using a gradient with an initial 1-minute hold at 30% B along with a 9-minute linear gradient from 30 to 95% B. Two compounds, urobilin and urobilinogen, were used to indicate the presence of the fecal matter with retention times of approximately 6.5min containing the m/z 343 and 8.5min containing the m/z 466 respectively. This was utilized to link the flies to pathogen transmission via fecal matter. Mentors: Nicholas Manicke, Department of Chemistry, Indiana University-Purdue University Indianapolis; Christine Skaggs, Department of Chemistry, Indiana University-Purdue University Indianapolis. Perinatatal Expression of DYRK1A in Male and Female Down Syndrome Mice Opeibea A. Aidoo12, Laura Hawley2and Randall J. Roper2, 1LSAMP Scholar; and2Department of Biology, Indiana University-Purdue University Indianapolis Down syndrome (DS), a genetic disorder that affects 1/700 live births is caused by the triplication of human chromosome 21(Hsa21) and is characterized by cognitive and skeletal deficits. One of the trisomic genes involved in DS is Dual specificity tyrosine regulated kinase 1A(DYRK1A). Triplication of genes on Hsa21has been proposed to cause an increased gene product and hence protein over expression. However, preliminary data suggests expression is not the same across ages and tissues. The hypothesis of this study is that trisomic DYRK1Aexpressionis differentially regulated spatially and temporally at the perinatal stage, and exhibits sexual dimorphism at the perinatal stage, which may contribute to cognitive deficits in DS. To quantify the perinatal (embryonic day 18.5(E18.5) to postnatal day 6(P6)) expression of DYRK1A, the Ts65Dn DS mouse model was used. The Ts65Dn mouse model contains a freely-segregating segmental trisomy of mouse chromosome 16 (Mmu16) and carries half the gene orthologs from Hsa21, including DYRK1A.Ts65Dn is the most widely used mouse model of DS and exhibits similar phenotypes as individuals with DS. Protein from E18.5 and P6 Ts65Dn and littermate control mice was isolated from the hippocampus, cerebral cortex, and cerebellum. Genotyping of all mice was accomplished by PCR. Bradford assays and Western blotanalys is were used to quantifyproteinandDYRK1Aexpression.Resultingdata suggests similar DYRK1A expression at E18.5 and increased DYRK1A expression at P6 in Ts65Dn as compared to euploid litter mates. These results suggest that treatments targeting DYRK1A activity at these sensitive stages of development when DYRK1A is overexpressed in trisomy could result in a reduction of DS-related cognitive deficits. Mentor: Randall J. Roper, Department of biology, IUPUI 1 Establishment of the Role of Aberrant Tau Oligomer Interactors on Toxicity In Vivo. Elysabeth Allman¹’³, Abby Perkins¹’², Yingjian You¹’², Yanwen You¹’², Tyler McCray¹’², and Cristian Lasagna-Reeves¹’² Stark Neurosciences Research Institute, 2Department of Anatomy and Cell Biology, IU School of Medicine, 3Purdue School of Science The microtubule-associated protein tau is responsible for microtubule assembly in neurons. The hyperphosphorylation of tau is thought to be the cause of tau accumulation and aggregation in the form of oligomers. Connections between the accumulation of toxic tau oligomers and neurodegenerative tauopathies, including dementias such as Alzheimer’s Disease (AD), have been established repeatedly, however it has yet to be determined whether or not the neurotoxicity observed in these diseases is solely produced by tau oligomers or these oligomers conjoined with other molecular interactors. The first goal of this project was to correlate a specific phosphorylation in tau with its accumulation in a mouse model for tauopathies that over-express human tau with the P301S mutation. To do so, immunohistochemical staining was performed using various antibodies that recognize tau phosphorylated sites. I used the AT8 antibody that recognizes tau phosphorylated at Ser202/Thr205, the PHF1 antibody that recognizes tau phosphorylated at Ser396/Ser404, the PHF6 antibody that recognizes tau phosphorylated at Thr231, and the S214 antibody that recognizes tau phosphorylated at Ser214. Staining revealed tau deposits present throughout the hippocampal and neocortical regions and prevalence was positively correlated with mouse age, indicating progressive neurodegeneration in these regions. Tau phosphorylated at Ser214 was found to correlate most closely with disease progression in the tauopathy mouse models. Mentors: Cristian Lasagna-Reeves, Department of Anatomy and Cell Biology, IU School of Medicine Influence of Astrocytes on Retinal Ganglion Cell Maturation andDisease When Derived from Human Pluripotent Stem Cells AnnaR. Allsop1, Kirstin VanderWall1, Ridhima Vij1, Kang-Chieh Huang1, Akshayalakshmi Sridhar1, Kelly Lentsch1, Theodore R. Cummins1-2, Jason S. Meyer1-3 1Department of Biology, Indiana University Purdue University Indianapolis;2Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN 46202;3Department of Medical and Molecular Genetics, Indiana University School of Medicine. Astrocytes are the most numerous types of cell in the central nervous system and perform numerous roles such as supporting neurons, supplying nutrients, providing mechanical support, maintaining ion balance, and aiding in synaptogenesis. During retinal development, astrocytes enter through the optic nerve and migrate into the nerve fiber layer. Retinal astrocytes perform similar functions as listed above and reside in close association with retinal ganglion cells (RGCs). Human pluripotent stem cells (hPSCs)can be utilized for modeling retinal cell types, including astrocytes and RGCs.This is done by differentiating hPSCs into astrocytes and RGCs using established protocols. This protocol was used to observe wildtype (WT)astrocyte development and their characteristics compared to glaucoma astrocytes in order to determine any disease phenotypes. The growth of the astrocytes was measured using ICC through the expression of astrocyte-specific proteins including
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