Scholarly Commons @Augusta University

 

Scholarly Commons is Augusta University's institutional repository and aims to preserve and distribute scholarly works and historical documents generated by the University and its legacy institutions. Scholarly Commons is managed by the University Libraries. For more information about the repository, please see the About page or contact Jennifer Davis, Scholarship and Data Librarian, at jdavis14@augusta.edu

 

                                             

 

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AU COVID-19 Research and Scholarship [99]
AU Open Access Pilot Program Awards [8]
AU Syllabi Repository [1]
AU Teaching Commons [6]
Wellstar MCG Health (formerly AU Health) [4]
University Publications [38]
Special Collections and Archives [2339]
  • IRON, COPPER, NICKEL, AND ZINC ION CONCENTRATIONS IN RAE’S CREEK

    Bridgers, Aerial; Augusta State University Honors Thesis; Augusta State University Honors Thesis (Augusta University, 2019)
  • Optimizing Isolation and Culture of Primary Microglia

    Doughty, Deanna; Augusta State University Honors Thesis; Augusta State University Honors Thesis (Augusta University, 2019)
  • You Should Know: Writing about Sexuality as a Woman

    McCarty, Kirsten; Augusta State University Honors Thesis; Augusta State University Honors Thesis (Augusta University, 2019)
  • Effects of Vitamin D Receptor Knockout, Vitamin D Deficiency, and Diabetes on Corneal Epithelial Nerve Density

    Vick, Sarah; Augusta State University Honors Thesis; Augusta State University Honors Thesis (Augusta University, 2019)
    This project is designed to test the hypothesis that vitamin D deficiency exacerbates preexisting primary corneal pathologies. Our lab has established that the corneal epithelium in diabetic mice heals at a faster rate than the epithelium in diabetic vitamin D receptor (VDR) knockout (KO) mice. It is known that within diabetic mice, the corneal nerve density is decreased, and it has been hypothesized that the decreased nerve density can slow corneal epithelium healing within mice. However, it is unknown how VDR KO or vitamin D deficiency in diabetic mice will affect corneal nerve density. In order to determine if nerve density is affected by VDR KO or vitamin D deficiency, mouse corneas were collected, nerves were immuno-stained for confocal microscope photography, and images were analyzed by image processing to determine nerve density. The results demonstrate that in otherwise healthy vitamin D deficient and VDR KO mice lacking the diabetic condition, nerve density was not affected by either vitamin D condition. Corneal nerve density was significantly decreased when vitamin D deficiency or VDR KO was combined with diabetes, confirming the hypothesis that vitamin D deficiency does worsen preexisting corneal pathologies. In addition, this finding may provide an explanation as to why diabetic VDR KO mice have delayed epithelial wound healing compared to control diabetic mice.
  • Small and Dangerous: MicroRNA-21 and Blindness

    Rajpurohit, Shubhra; Augusta State University Honors Thesis; Augusta State University Honors Thesis (Augusta University, 2019)
    Background: Retinal and choroidal neovascularization (RNV and CNV, respectively) are characterized by the inappropriate growth of retinal capillaries that may progress to retinal scarring, detachment and vision loss. MicroRNAs (miRs) are short noncoding RNAs which have been demonstrated to modulate diverse cellular processes such as cell differentiation, proliferation, and apoptosis. Our group and others have shown that miR-21 plays a crucial role in regulating angiogenesis and neovascularization in retina. We have previously shown that activation of STAT3/miR-21 pathway leads to loss of TIMP3 and activation of MMP2 and MMP9. Increased activity of MMP2 and MMP9 in the ischemic retina has been linked to the proteolytic degradation of pigmented epithelial derived factor (PEDF), a key retinal angiostatic factor. Importantly, miR-21 targets peroxisome proliferator-activated receptor alpha (PPARα). PPARα-responsive elements are found in PEDF promoter suggesting that this could be a potential transcription factor for PEDF. The role of miR-21 in regulating PEDF and PPARα in Human Retinal Pigmented Epithelial cells (HuRPE) has never been investigated and is the main goal of the present study. Methods: HuRPE were treated with VEGF at different time points. Transfection of HuRPE cells was performed using a specific miR-21 inhibitor, a miR-21 mimic, and scrambled miRNA as a negative control. Western blot and real-time PCR were used to evaluate the expression of PEDF and PPARα. Luciferase assay was performed to study the interactions between PPARα and PEDF. Results: VEGF treatment of HuRPE cells promoted the expression of miR-21 while PEDF and PPARα expression was down regulated. Further, overexpression of miR-21 decreased PEDF and PPARα expression. Next, we observed that inhibiting miR-21 expression could rescue VEGF-induced down regulation of PEDF and PPARα. To study the specific relationship between PPARα and PEDF, we treated HuRPE cells with siPPARα (inhibition) or PPARα agonist (fenofibrate) (induction). While, inhibition of PPARα expression decreased PEDF expression, PPARα agonist enhanced PEDF 5 expression. Lastly, using a PEDF promoter plasmid we observed that, PPARα could regulate PEDF expression by modulating its promoter activity. Conclusion: Collectively, our data shows that VEGF-mediates induction of miR-21 expression regulates PPARα-PEDF axis and could have a significant role in choroidal neovascularization. This suggests that miR-21 potentially plays a critical role in age-related macular degeneration. Keywords: Retinal Neovascularization, MicroRNA-21, PEDF, and PPARα

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