Now showing items 21-40 of 5421

    • The effect of mineralocorticoid receptor antagonism on ischemic infarct size and cerebral vessel structure in male and femail spontaneously hypertensive stroke-prone rats: sex difference revealed.

      Rigsby, Christine Spring; Medical College of Georgia (Augusta University, 2006-12)
      Stroke is the third leading cause of death ·and the leading cause of long-term disability in the United States, where approximately 88% of stroke occurrences are ischemic in origin. Hypertension is a primary risk factor for stroke. Elevated aldosterone levels have also been identified as a risk factor for stroke, as patients with primary aldosteronism incur increased incidences of cardiovascularrelated pathologies than do patients with essential hypertension. Previous studies from our laboratory have shown that mineralocorticoid (aldosterone) receptor (MR) activation can induce deleterious vascular remodeling and, conversely, blockade of the MR with spironolactone reduces cerebral infarct size in male spontaneously hypertensive stroke-prone rats (SHRSP). It is known from studies in SHRSP that cerebral vessel structure is directly related to infarct size. We hypothesized that chronic spironolactone treatment would alter cerebral vessel structure. Six-week-old male SHRSP were treated with spironolactone for six weeks and passive vessel structure was analyzed using a pressurized arteriograph. Spironolactone treatment prevented cerebral vessel remodeling. From a clinical standpoint, many patients present with pre-existing vascular damage; therefore, we hypothesized that chronic MR antagonism would reverse existing vascular damage. Twelve-week-old male SHRSP were treated as described above. Interestingly, spironolactone treatment partially reversed existing cerebral vessel remodeling. Recent analysis of data from the Framingham Heart Study show that females may be more sensitive to the effects of aldosterone, but few studies looking at MR blockade have been performed in females. Similar ischemic stroke and vascular analysis studies were performed in 12-week-old female SHRSP. Contrary to the male studies, MR antagonism, using spironolactone or eplerenone, did not reduce damage from ischemic stroke or improve vessel structure. MR protein expression was evaluated in cerebral arteries collected from 12-week-old male and female SHRSP using Western blot analysis. Surprisingly, female SHRSP had increased MR expression, compared to male SHRSP. These novel studies uncover an apparent sexual dimorphism in the actions of MR antagonists and expression ofthe.MR in SHRSP. The action of the MR antagonists may be influenced by differential MR expression and this could help to explain the sex difference observed. existing cerebral vessel remodeling. Recent analysis of data from the Framingham Heart Study show that females may be more sensitive to the effects of aldosterone, but few studies looking at MR blockade have been performed in females. Similar ischemic stroke and vascular analysis studies were performed in 12-week-old female SHRSP. Contrary to the male studies, MR antagonism, using spironolactone or eplerenone, did not reduce damage from ischemic stroke or improve vessel structure. MR protein expression was evaluated in cerebral arteries collected from 12-week-old male and female SHRSP using Western blot analysis. Surprisingly, female SHRSP had increased MR expression, compared to male SHRSP. These novel studies uncover an apparent sexual dimorphism in the actions of MR antagonists and expression ofthe.MR in SHRSP. The action of the MR antagonists may be influenced by differential MR expression and this could help to explain the sex difference observed. existing cerebral vessel remodeling. Recent analysis of data from the Framingham Heart Study show that females may be more sensitive to the effects of aldosterone, but few studies looking at MR blockade have been performed in females. Similar ischemic stroke and vascular analysis studies were performed in 12-week-old female SHRSP. Contrary to the male studies, MR antagonism, using spironolactone or eplerenone, did not reduce damage from ischemic stroke or improve vessel structure. MR protein expression was evaluated in cerebral arteries collected from 12-week-old male and female SHRSP using Western blot analysis. Surprisingly, female SHRSP had increased MR expression, compared to male SHRSP. These novel studies uncover an apparent sexual dimorphism in the actions of MR antagonists and expression ofthe.MR in SHRSP. The action of the MR antagonists may be influenced by differential MR expression and this could help to explain the sex difference observed.
    • Herpesvirus prevalence and methylation status in ganglia of the human head and neck

      Richter, Elizabeth R.; Medical College of Georgia (Augusta University, 2008-07)
      The neurotropic human alphaherpesviruses, herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) and varicella-zoster virus (VZV), are latent in a majority of the adult population. These viruses can reactivate to cause many diseases (e.g. herpes labialis, shingles) and sometimes unusual clinical sitespecific neurological syndromes ranging from neuralgia to deadly encephalitis. Although the trigeminal ganglion has been thought to be the main site of reactivation, additional sensory and autonomic ganglia contain viral genomes. A comprehensive study of these additional sites of latency and their respective viral burden is needed to understand the full spectrum of latency and possible sites of viral reactivation in humans. While animal models of HSV provide some insight into the pathogenesis of herpesvirus infections, they do not provide information about the prevalence and characteristics of these viruses in their natural host. The overall goal of this study was to elucidate the distribution of the neurotropic human herpesviruses and to determine whether ganglionic positivity at one site in the head and neck correlated with virus presence in ipsilateral and/or contralateral sites. By using formalin-fixed tissue from human cadavers, we were able to: 1) investigate the frequency and correlation of genomes in 8 ganglia on each side of the head and neck, and 2) determine whether latent virus exists in a methylated state. From these studies, we now have a more complete characterization of latency patterns in the human head and neck. This thorough comparison among 16 ganglia around the head and neck provided a more comprehensive perspective of the pattern of latency and by extrapolation, of sites of possible reactivation. The results of these studies suggest that HSV-1 and VZV (but not HSV-2) are independently distributed among ganglia of the human head and neck and that DNA methylation of the HSV-1 genome is not a likely epigenetic mechanism in latently infected human ganglia. An expanded knowledge of latency sites, prevalence of latency, and epigenetic mechanisms of latent viruses in the head and neck may provide insight into the pathogenesis of herpesvirus infection in unusual sites. Such knowledge may also be used to develop approaches to reduce or prevent reactivation or to ameliorate the effects of herpesvirus infections of the head and neck.
    • Musculoskeletal disorders in Georgia sonographers

      Yeyes, Lynn K.; Medical College of Georgia (Augusta University, 2001-03)
    • CJ0596 plays a role in the virulence of campylobacter jejuni

      Rathbun, Kimberly M.; Doctor of Philosophy (Augusta University, 2009-05)
      Campylobacter jejuni is a gastrointestinal pathogen of humans but part of the normal flora of poultry. C. jejuni therefore grows well at both 37°C and 42°C. Proteomic studies on temperature regulation in C. jejuni strain 81-176 revealed the upregulation at 37°C of Cj0596, a predicted periplasmic chaperone that is similar to proteins found to be involved in outer membrane protein (OMP) folding and virulence in other bacteria. The cj0596 gene was highly conserved in multiple strains and species of Campylobacter (24 in total), implying the importance of this gene. To study the role Cj0596 plays in Campy/obacter pathogenesis, a mutant derivative of strain 81-176 was constructed in which the cj0596 gene was precisely deleted. This mutant was complemented by restoring the gene to its original chromosomal location. The mutant strain demonstrated a decreased growth rate and lower final growth yield, yet was more motile than wild-type. The cj0596 mutant also showed altered levels of several outer membrane proteins (OMPs), and changes in membrane-associated characteristics (antimicrobial sensitivity, autoagglutination, and biofilm formation). In either single or mixed infections, the mutant was less able to colonize mice than wild-type. Purified, recombinant Cj0596 had peptidyl-prolyl cistrans isomerase (PPiase) activitty, but did not functionally complement an E. coli surA mutant. These results suggest that C. jejuni Cj0596 is a PPiase and loss of Cj0596 alters phenotypes that have been shown to be related to the pathogenesis of the bacterium.
    • Physiological consequences of ENOS subcellular targeting

      Qian, Jin; Medical College of Georgia (Augusta University, 2012-01)
      Anti-inflammatory effects of NO are thought to involve inhibition of the proinflammatory transcription factor, NF-KB. NO represses the nuclear translocation ofNFKB via the S-nitrosylation of its subunits which decreases the expression of target genes including adhesion molecules. We next investigated the significance of subcellular targeting of eNOS to NF-KB signaling induced by proinflammatory cytokines in human aortic endothelial cells (HAECs). We found that in HAECs stimulated with TNFu, LNAME did not influence the expression of ICAM-1 or VCAM-1. In eNOS "knockdown" HAECs, reconstituted with either PM- or Golgi- restricted forms of eNOS, there was no significant effect of endogenously produced NO on the activation of the NF-KB pathway in response to different concentrations and exposure times of TNFu. Similarly, the endogenous production of NO did not influence the phosphorylation of IkBu and Snitrosylation of IKKP or p65. In contrast, higher concentrations of NO, derived from the use of the exogenous NO donor, DETA NONOate, effectively suppressed the expression of ICAM-1NCAM-1 in response to TNFu and induced more S-nitrosylation of IKKP and p65. These results suggest that neither endogenous eNOS nor eNOS location is an important regulatory influence on inflammatory signaling in HAECs via the NF-KB pathway and that higher NO concentrations are required to suppress NF-KB. A third focus of non-cGMP NO signaling was the NADPH oxidases (Nox), a family of transmembrane oxidoreductases that produce superoxide and other reactive oxygen species (ROS). There are 5 family members (Noxl-5) with Nox5 the last of the conventional Nox isoforms to be identified. Nox5 is a calcium-dependent enzyme that does not depend on accessory subunits for activation. Recently, Nox5 was shown to be expressed in endothelial cells in human blood vessels and therefore we investigated whether endogenous levels of NO can influence Nox5 activity and if so to identify the mechanisms involved. We found that endogenous NO was a potent inhibitor of basal and stimulated Nox5 activity and inhibition was reversible with chronic, but not acute exposure to L-NAME. Nox5 activity was reduced by NO donors, iNOS, eNOS and in endothelial cells and cytokine-stimulated smooth muscle cells in a manner proportional to the NO concentration. ROS production was diminished by NO in an isolated enzyme activity assay replete with surplus calcium and NADPH. There was no evidence for NOdependent changes in tyrosine nitration, glutathiolation or phosphorylation of Nox5 and ROS production was not modified by GAPDH. In contrast, there was evidence for the increased nitrosylation of Nox5 as .determined by the biotin-switch assay and mass spectrometry. Four S-nitrosylation sites were identified and of these, mutation of C694 dramatically lowered Nox5 activity, NO-sensitivity and biotin-labeling. Furthermore, coexpression of the denitrosylation enzymes thioredoxin (Trxl) and GSNO reductase (GSNOR) prevented NO-dependent inhibition ofNox5. The potency of NO against other Nox enzymes was Noxl:;::Nox3>Nox5>Nox2 whereas Nox4 was refractory. These results demonstrate that endogenously produced NO can directly S-nitrosylate and inhibit the activity ofNox5. The overall conclusion of these studies is that the amount of NO is the most important variable influencing protein S-nitrosylation and function.
    • A counseling intervention to improve personal control, affective outcomes, and satisfaction in surrogate decision makers at end-of-life

      Purvis, Reese J.; Medical College of Georgia (Augusta University, 2006-02)
      This study investigated whether personal control, situational anxiety, situational depression, and satisfaction with end-of-life (EOL) care might be improved in surrogate decision makers who receive a cognitive-behavioral decision making intervention. The sample consisted of 38 surrogate decision makers for 38 incapacitated patients in three hospitals in a moderate sized city in the. Southeastern United States. The demographic characteristics of sample included: 50% female and 50% male, 50% African-American and 50% White, and 81.6% Protestant. Although the sample was small, the demographic composition of the sample was highly consistent with the population of the community in which the study was conducted. Guided by Bandura's Social Cognitive Theory, it was hypothesized that experimental (DMCI) group subjects would score higher on posttest measures of personal control and satisfaction with EOL care than subjects in the usual care group. It was also hypothesized that experimental group subjects would score lower on posttest measures of depression and anxiety. Pretest and posttest scores on five instruments were compared and analyzed for an experimental group, N=19 which received the DMCI versus a control group, N= 19, that received only usual care. Instruments used to assess the dependent variables of personal control, affective outcomes, 3!1d satisfaction with end-of-life care were: the Pearlin Mastery Scale, the Perceived Personal Control Questionnaire, the Beck Depression Inventory, the Beck Anxiety Inventory, and the FAMCARE Scale. Data were collected over a seven month period from Summer 2004 to Spring 2005. After obtaining informed consent experimental participants completed all instruments (pretest), received three counseling sessions over approximately 14 days and then completed all instruments again (posttest). Control group members after providing informed consent also completed all instruments (pretest), received three attention- usual care contacts, and subsequently completed all instruments again (posttest). Data were analyzed using descriptive statistics, Chi-Square, Mann-Whitney Test, and 2-way ANOV A with one repeated measure. The factors were group assignment (experimental vs. control) and time (pretest vs. posttest) with time as the repeated factor. Chi-square, and Mann-Whitney tests showed the groups were comparable at pretest and that demographically the random assignment to groups was effective. The 2-way ANOV A results showed significant interaction effects in each case. The experimental group scored higher or lower posttest as predicted by the hypotheses compared to the control group.
    • Effect of a novel calcium phosphate coating on osseointegration of titanium implants: a study in rabbits

      Poulos, Nicholas; Medical College of Georgia (Augusta University, 2008-01-15)
    • Impact of genetic predisposition and environmental stress on measures of preclinical essential hypertensio

      Poole, Joseph Christian; Jospeh, Poole; Medical College of Georgia (Augusta University, 2008-06)
      The main objective of this project was to determine the impact of genetic risk and chronic environmental stress on measures of preclinical essential hypertension (EH) (e.g., exaggerated cardiovascular reactivity, increased resting hemodynamics and increased left ventricular mass [LVM]). A secondary objective was to evaluate the moderating and interactive effects of ethnicity, gender, body mass index [BMI] and anger expression on EH risk indices. Two genes with relevance for blood pressure (BP) control (e.g., beta-2 adrenergic receptor [ADRB2] gene and serotonin transporter [5-HTT] gene) were used to define genetic risk. Chronic environmental stress was assessed by socioeconomic status (SES) and subjective social status (SSS). The project consisted of three sequential studies on a large, multiethnic cohort of young adults (N>500). The first two studies were cross-sectional and based on the analysis of cardiovascular reactivity, resting hemodynamics and LVM data collected at a single visit. The third study was longitudinal and involved the tracking of BP and LVM over a 15-year span from childhood to early adulthood. In the first study, ADRB2 haplotype significantly interacted with anger suppression in African Americans such that high anger suppressing carriers had the highest resting SBP (p<.05) and TPR reactivity to a cold pressor task (p<.01 ). In European Americans, ADRB2 'haplotype significantly interacted with BMI to predict resting hemodynamics, such that carriers who were high in BMI showed the highest SBP (p<.05). In the second study, a significant interaction between the 5-HTI promoter region polymorphism (5-HTILPR) and social status was found for cardiovascular reactivity, such that S allele homozygotes who were low in SES and high in SSS exhibited the greatest BP and TPR reactivity to the video game stressor (p-values<.05). No significant interaction was found between 5- HTILPR and social status in the longitudinal study, however a significant 5- HTILPR by BMI interaction was determined for LVM, such that obese LL homozygotes had the greatest LVM over time (p<.001 ). Results from this project expand what is currently known with regard to EH etiology and carry implications for the prevention of EH through the early consideration of genetic, environmental and demographic risk factors.
    • MYR 8 : the first member of a novel myosin class is expressed during brain development

      Patel, Krishna Gwynne; Medical College of Georgia (Augusta University, 2000-05)
      Neuronal cell migration and cellular differentiation, major phases in the assembly process of the mammalian neocortex, involve considerable organelle and cellular motility. While the cytoskeletal organization of migrating neurons is well documented, and the involvement of the cytoskeleton in modulating intracellular membrane transport events during neuronal cell differentiation is well appreciated, identification of selective cytoskeletal components underlying these· processes is only beginning to emerge. Observations over the past two decades reveal that myosin motors are involved intimately in multiple actin-dependent membrane movements, including vesicular trafficking, organelle localization and organization, endocytosis, exocytosis, phagocytosis, lamellopodial extension, and the more classically defined functions such as cytokinesis, contractility, and cell motility or migration. Accordingly, our studies have been directed toward the identification and characterization of unconventional myosins that may participate in neuronal cell migration and/or differentiation events within the developing manlinalian brain. Our analyses identified two myosin isoforms that contribute to a novel unconventional myosin class. We have cloned, sequenced, and designated these myosin isoforms as myr Sa and Sb (S,. unconventional myosin from rat). Structurally, the head domain of myr & contains a large N-terminal extension composed of multiple ankyrin repeats similar to· myosin phosphatase. The motor domain is followed by a single putative light chain binding domain. The tail domain of myr Sa is comparatively short with a net positive charge, whereas the elongated tail domain of myr Sb bears an overall neutral charge and reveals several streches of poly-proline residues. Phylogenetic analysis indicates that myr 8 is sufficiently divergent from known myosins as to comprise a new class of myosins. Northern. analyses demonstrate that the myr 8 myosins are expressed predominantly in the nervous system, and are detected principally at developmental timeperiods. Indirect-immunofluorescent studies reveal a pattern of irmnunoreactivity within forming neuronal and astroglial cell processes located throughout the ·developing brain. Taken together these data suggest that this novel myosin may play a crucial role in membrane biogenetic events during neuronal and astroglial cell differentiation. Given the increasing identification of neurological dysfunctions that arise as a consequence of defective myosins, as well as from other cytoskeletal components, it is essential to unravel the selective roles in which this novel unconventional myosin may participate during neocortical development.
    • Development of DNA probes for the detection of endodontic pathogens

      Pantera, Carole T; Department of Oral Biology (Augusta University, 1993-08)
    • The level of loneliness experienced by adolescent mothers related to social support and locus of contro

      Paisley, Janet A.; School of Nursing (Augusta University, 1991-05)
      The purpose of this study was to examine whether there was a relationship between the level of loneliness. the degree of social support, and perceived locus of control of adolescent mothers. An ex-post facto correlational design was used in this study to examine whether there was a relationship between the variables. Results of this study revealed no significant relationships between level of loneliness, so~ial support, and locus of control. However, when social support was broken down into family total functional support and peer total functional support, some significant relationships were found. Family support was found to be related to decreased levels of loneliness for adolescent •others. Peer support was found to have a curvilinear relationship with loneliness, demonstrating that increasing peer suppori is associated with ·decreasing loneliness until a certain point, beyond which loneliness increases.
    • Vascular Effects of β-Amyloid in Alzheimer's Disease

      Ozcan, Ozan; Medical College of Georgia (Augusta University, 2006-08)
    • T cell immune response in persistent infection of lymphocytic choriomeningitis virus (LCMV

      Ou, Rong; Medical College of Georgia (Augusta University, 2004-07)
      The murine LCMV system provides a classic model to study the mechanism of immunological tolerance, an efficient strategy used by virus to establish a persistent infection by selective down-regulation of virus-specific T lymphocytes. High viral burden in the onset of infection drives responding cells into functional unresposiveness (anergy) that can be followed by their physical elimination. In this study, the downregulation of the virus-specific CDS+-T -cell response was' studied during a persistent infection of adult mice, with particular emphasis on the contribution of the interferon response in promoting host defense, or perforin-, Fas/FasL-, or TNFRI-mediated cytolysis in regulating T -cell homeostasis. Since LCMV infects a broad range of host tissues, the functional properties of virus-specific CDS+ T cells in different tissues during LCMV infection were also evaluated. Infection of mice deficient in receptor for type I (IFN-a/~), type II (IFN-y), or both type I and II IFNs with LCMV isolates that vary in their capacity to induce T -cell exhaustion, revealed a critical role for IFN-a/~ in restricting LCMV spread at the onset of infection while IFN-y has impact on effector cells. The production of IFN-a./~ and/or IFN-y critically regulates the virus-host balance during the acute phase of infection, such that a high viral burden drives responding cells into different programs of exhaustion. Infection of mice deficient in perferin, FasL or TNFRI with the Docile or Aggressive strains of LCMV revealed comparable kinetics of expansion and functional inactivation of virusspecific CDs+ T cells in the early phase of infection in C5 7 BL/6 controls. However, the data underscore a critical role for these molecules in the persistence of the virus-specific ens+-T-cell population once it has become anergic. Study of the functional properties of virus-specific ens+ T cells in different tissues during LeMV infections showed that a central role for the viral load in lymphoid tissue in the induction and maintenance of clonal exhaustion. The <;lata strongly suggest that ens+ T cells may be differentially regulated in the environments of lymphoid versus nonlymphoid tissues, and the pattern of T cell exhaustion observed with mice is likely a common feature ofthe immune response during chronic infections in humans.
    • Plasma membrane disruption in orthodontic tooth movement

      Orellana, Maria Fernanda; Medical College of Georgia (Augusta University, 2002-04)
    • Investigating the Functions of Tinagl1 in Embryonic Development

      Zwinklis, Brooklyn; Department of Biological Sciences (Augusta University, 2020-12)
      This research project was designed to explore the functions of Tubulointerstitial Nephritis Antigen-Like protein 1 (Tinagl1) in embryonic development. Prior work using morpholino knockdowns in zebrafish suggested that downregulating the tinagl1 gene has profound effects on development, resulting in defects including small eyes, body axis curvature, renal cysts, missing craniofacial cartilages, and reversed heart looping. Several of these defects could result from observed shortening and reduction in the number of motile cilia. However, morpholino knockdown techniques have fallen out of favor in zebrafish research and have been replaced by gene editing methods, such as Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR), to completely remove gene function throughout the embryo permanently. This project seeks to further test the function of tinagl1 on development through two independent and current approaches. The first approach will seek to validate or refute the prior morpholino results by knocking out tinagl1 via a 4-guide CRISPR method as it is described by Wu et al. The second approach will examine if overexpression of an engineered tinagl1 mutant mRNA can result in a dominant-negative effect that causes all the previously mentioned defects with the addition of asymmetrical craniofacial defects. These approaches will help establish Zebrafish animal models for studying functional requirements for Tinagl1 and its interactions with signaling pathways.
    • Ray Abundance and Diversity in the Satilla River

      Silliman, Brennan; Department of Biological Sciences (Augusta University, 2020-12)
      Over the past 100 years, the Satilla River has been cut several times for logging and navigational purposes. The most notable cut is Noyes Cut, located adjacent to Umbrella and Dover Creeks. Due to changes in local economic pursuits, Noyes Cut is not used except by a few local fishermen and has potentially altered water flow and salinity gradients. Ultimately, this affects habitats of animals, such as rays. The Satilla River is home to 52 different kinds of species of saltwater and freshwater fish. These include sunfish, sharks, catfish, seatrout, and tarpon (Kenakrow, 2020). Rays are found worldwide and are the most diverse of cartilaginous fish; they play a vital role in determining the health of an ecosystem by influencing/controlling where certain fish, mollusk, and crustacean populations are. Rays can indicate if an ecosystem is in distress. Four locations in the Satilla River were sampled using experimental gill nets, otter trawls, and a multi-parameter water quality probe from July 2014 through September 2019. All rays were identified by species with total length and disc width recorded to the nearest centimeter (cm). At least 3 species of rays (possibly more), which include the Atlantic Stingray, the Smooth Butterfly Ray, and the Southern Stingray, call this area home. Additionally, this five year data set will be compared to a creel survey currently being conducted on the Satilla River. We hope to make comparisons between our 2018-2019 sampling year and the 2019-2020 creel survey. Since rays are an indicator species, it may be possible to determine if they’ve been affected by Noyes Cut. Noyes Cut was originally constructed around 1910 as a way for Edward Noyes to float logs to his lumber mill business. He used this waterway until 1933 when the U.S. Army Corps seized it and deepened the cut as an inland waterway. Over several decades, channel sedimentation has gradually affected salinity gradients which ultimately altered the natural water circulation patterns within the estuary.
    • Mechanism of Retinal Neovascularization in OIR: Role of ACAT-1

      Santana, Isabella Noel; Department of Biological Sciences (Augusta University, 2020-12)
      According to the National Eye Institute, Retinopathy of Prematurity (ROP) is the leading cause of vision loss in childhood. About 400–600 infants each year in the US become legally blind from ROP (NIH, 2019). ROP primarily affects premature infants weighing less than 2.75 pounds who are born before thirty-one weeks of gestation (NIH, 2019). Today, with the advances being made in neonatal intensive care, smaller premature infants are being saved. Because these infants are at a much higher risk for ROP, it has become increasingly important to understand ROP. ROP affects the blood vessels in the retina, which is the thin layer of tissue that lines the back of the eye and is responsible for receiving light and converting it into neural signals. Loss of vision occurs when abnormal blood vessels grow and spread throughout the retina and into the vitreous, developing neovascular tufts, causing hemorrhage. Retinal detachment is the main cause of visual impairment and blindness in ROP (NIH, 2019). The primary current treatments are laser therapy and anti-vascular endothelial growth factor (VEGF), but these therapies have shown negative side effects and complications associated with them being invasive procedures such as intraocular swelling, retinal detachment and infectious endophthalmitis (Dowler, 2003). The mechanism behind retinopathy of prematurity is unclear, however; macrophage proliferation has been found to have a critical role in the development of retinal neovascularization by secreting growth factors and inflammatory cytokines such as VEGF, Interleukin 6 (IL-6), Monocyte colony stimulating factor (MCSF) and trigger receptor expressed on myeloid cells (TREM-1) (Zhou, et al. 2017). The manner in which macrophages are activated for this process is also unknown, however; lipid metabolism is vital for maintaining macrophage homeostasis and function. Lipid loading in macrophages increases intracellular cholesterol esters (CEs), which induce an inflammatory phenotype. Acyl coenzyme A: cholesterol acyltransferase-1 (ACAT-1) is an enzyme localized in macrophage endoplasmic reticulum that is responsible for cholesterol esterification with fatty acids and the formation of CEs. Our preliminary results in wild-type (WT) mice pups treated with intraperitoneal injections (I.P.) of ACAT-1 inhibitor in a model of oxygen-induced retinopathy show significant decrease of retinal neovascularization, avascular area and expression of TREM-1, M-CSF and VEGF. We hypothesize that ACAT-1 activityderived high cholesterol levels in macrophages during hypoxia induce retinal neovascularization.