• Erica Joan Pruett Anderson, BS

    Graduate Student, Cone laboratory, Molecular Physiology & Biophysics

    My research project is focused on advancing our understanding of the molecular and kinetic mechanisms of energy maintenance by elucidating if and when MC4R induced Kir7.1 signaling is required for regulation of food intake and energy expenditure.  We believe MC4R functions as a rheostat of energy maintenance by utilizing both tissue specific Gαs and Kir7.1 signaling modalities as well as unique kinetic aspects of these modalities.  I am using an in vivo  modeling system to test this hypothesis.

    8435 MRB IV
    (615) 936-8144 (lab)

  • Caleigh Mariko Azumaya, BS

    Graduate Student, Terunaga Nakagawa lab, Molecular Physiology and Biophysics

    AMPA receptors (AMPARs) are ligand-gated cation channels whose appropriate activity and regulation are integral to most central nervous system function. They mediate the majority of excitatory neurotransmission and their dysregulation has been implicated in many cognitive disorders. My research focuses on the molecular details of auxiliary subunit interactions with the AMPAR. Using biochemical and structural biology techniques, we hope to illuminate the molecular basis of interaction between these two proteins and how that relates to the auxiliary subunit’s modulation of AMPAR in vivo.

    766 RRB (MRB I)

  • William Reid Bolus, BS

    Graduate Student, Alyssa Hasty laboratory, Molecular Physiology and Biophysics

    I study the role of eosinophils in adipose tissue homeostasis, specifically during periods of weight gain or weight loss. In particular, I seek to understand how eosinophils impact key aspects of adipose tissue physiology such as macrophage inflammatory state, vascularization, extracellular matrix remodeling, and adipocyte insulin sensitivity.

    Light Hall

  • Karin Janae Bosma

    Graduate Student, O'Brien laboratory, Molecular Physiology & Biophysics

    Elevated fasting blood glucose (FBG) levels have been associated with an increased risk of type 2 diabetes (T2D) development and cardiovascular-associated mortality (CAM). Genome-wide association studies (GWAS) have identified SNPs in G6PC2 associated with FBG. G6PC2 is an isoform of the glucose-6-phosphatase catalytic subunit expressed in pancreatic islet beta cells. Deletion of G6pc2 in mice results in reduced FBG, consistent with the human GWAS data, and islets from these mice have enhanced glucose-stimulated insulin secretion (GSIS) at sub-maximal glucose concentrations. I am using mouse models to explore the function of G6pc2 in islet beta cells and its potential as a therapeutic target for the prevention of T2D and CAM.

  • Sheridan Jared Carrington, BBMedSci

    Graduate Student, Cone and Mchaourab Laboratories, Molecular Physiology & Biophysics

    My thesis research aims to investigate how G protein-coupled receptors (GPCRs) regulate the trafficking of a novel ion channel, Kir7.1. Our lab has found that the GPCR melanocortin 4 receptor (MC4R), interacts with the Kir7.1 inwardly rectifying potassium channel to regulate energy homeostasis.  We have found that MC4R can modulate the activity of Kir7.1 independent of G-proteins, and my project seeks to identify the molecular basis for this interaction.

  • Matthew Cottam

    Graduate Student, Hasty laboratory, Molecular Physiology & Biophysics

  • Bethany Lyn Dale

    Graduate Student , Madhur Lab

    I study the role of interleukin-21(IL-21) in hypertension associated end-organ damage and dysfunction using an IL-21 global knockout mouse. I am looking at the presence and effector function of IL-21 producing cells in Angiotensin II induced experimental hypertension.

  • Joseph Elsakr, BSE

    Graduate Student, Gannon Lab

    A mother's diet and metabolic status during gestation has been shown to affect her offspring's risk of developing metabolic disease later in life. In the Gannon Lab, I study the mediators of this increased disease risk using two animal models of maternal high fat diet during pregnancy. In a collaboration with multiple labs across the country, I obtain pancreata from non-human primates exposed to high fat diet in utero. Pancreatic endocrine cell mass, structure, and function are currently being investigated. In a mouse model, I study the effects of maternal high fat diet on the epigenetic profile of pancreatic beta cells in the offspring. Together, these studies will enhance our understanding of how high fat diet during pregnancy predisposes offspring to develop metabolic disease. 

  • Slavina Goleva

    Graduate Student, Sweatt laboratory, Molecular Physiology & Biophysics

  • Andrew Young Gordon, BA

    Graduate Student, Penn laboratory, Molecular Physiology & Biophysics

    I research and create novel nanoparticles for molecularly targeted imaging of the eye. My project involves using gold nanorods as exogenous contrast agents in the eye that are compatible with optical coherence tomography systems. My research includes the construction of gold nanorods and their modification for stability and biocompatibility. I collaborate with researchers outside my lab to perform work related to photothermal optical coherence tomography. Additionally, my research focuses on methods of drug delivery to the eye. As this is imaging research, I use a variety of imaging modalities relevant to in vivo imaging of the eye, notably optical coherence tomography. 

  • Rachana Haliyur

    MD PhD Student, Al Powers laboratory, Molecular Physiology & Biophysics

    Recent observations have challenged long held concepts in the pathophysiology of type 1 diabetes. By implementing an integrative approach to study both the native pancreas and isolated islets from the same human donor, I work to characterize the function and morphology of T1D pancreatic islets using in vitro and in vivo functional studies and immunohistochemistry. My primary project focuses on the glucagon-producing alpha cells in the T1D islet and identifying the mechanisms behind disordered glucagon secretion in T1D. 

  • Nick Harris, BS

    MD PhD Student, Winder laboratory, Molecular Physiology & Biophysics

    Drug dependent patients trying to maintain abstinence often relapse to their chosen of drug of abuse, with many citing stress as an antecedent to use and a lack of effective treatment to control the urge to use. Guanfacine is an α2A-adrenergic receptor agonist that targets receptors for the brain stress neurotransmitter norepinephrine and has been used in both preclinical and clinical trials for addiction, often showing positive results such as reduced craving but not producing changes in ultimate rates of relapse. We hypothesize that the ineffectiveness on relapse is due to competition among the myriad effects of this drug and aim to study a non-canonical neuronal activating effect in the bed nucleus of the stria terminalis, an area of the brain known to be implicated in both stress and addiction disorders, through the complementary use of whole cell electrophysiology and neuroanatomical methods in the hopes that uncovering the mechanism underlying this effect will aid in future treatment of patients dependent on drugs of abuse.

    754 PRB
    (615) 714-9631

  • Merla Hubler, MS

    MD PhD Student, Hasty laboratory, Molecular Physiology & Biophysics

    I am studying the role of macrophages in maintaining iron homeostasis in adipose tissue. Specifically, we have identified a subset of resident macrophages that compensate for excess iron in the tissue. We are currently interested in depleting this population of macrophages in order to assess their importance in maintaining the health of adipocytes. In future studies we will address the importance of iron handling by macrophages in obesity, and the temporal distribution of iron in adipose tissue and liver tissues.

  • Kelli Jordan

    Graduate Student, Jacobson laboratory, Molecular Physiology & Biophysics

  • Ben Kesler, BS

    Graduate Student in the Neuert Lab

    The sequencing of genomes from many different organisms has shown that a large fraction of the genome is transcribed into RNA but does not code for proteins. Genome-wide studies have identified many long non-coding RNAs (lncRNAs), yet very little is known about their functions. The Neuert lab's previous studies have demonstrated that non-coding RNAs modulate the localization of key transcription factors, which influence the occurrence of downstream events that lead to active or silenced transcription. I will use a combination of quantitative single-molecule RNA experiments in single cells with genetic manipulations and single-molecule-based modeling to understand the molecular mechanism of transcriptional regulation of long non-coding RNAs in mammals to greater detail.

    813 Light Hall
    (615) 322-4610

  • Peter Allerton Kropp, BA

    Graduate Student, Gannon laboratory, Molecular Physiology & Biophysics

    I am interested in understanding the role of the transcription factor Oc1 (Onecut1) in pancreas development and disease. Oc1 is essential for development of the endocrine pancreas, so I am investigating its interaction its cofactor Pdx1 in that role. I have thus far determined that proper dosage of both Oc1 and Pdx1 is necessary for endocrine cell differentiation and that defects established during development persist into adulthood. I am further interested in identifying the direct targets of Oc1 during pancreas development since so little is known about its direct regulatory role.

    7435 MRB IV

  • Roxanna Loperena, BS

    Graduate Student, Harrison laboratory, Molecular Physiology & Biophysics

    In the past 20 years, two new mechanisms of hypertension have been defined: one is oxidative injury and the second is inflammation. Our lab has shown that dendritic cells (DCs) from hypertensive mice accumulate isolevuglandins that adduct to proteins and promote T cell activation. In hypertension, the endothelium is activated to produce reactive oxygen species and to express adhesion molecules and chemokines that attract inflammatory cells. In my project, we hypothesized that human endothelial cells exposed to mechanical stretch will promote conversion of human monocytes into activated DCs. Therefore, I study this conversion when monocytes co-cultured with human aortic endothelial cells exposed to either normal cyclical stretch (5%) or hypertensive cyclical stretch (10%) using the Flexcell® Tension System. I also study the different signaling molecules that could potentially be facilitating this process in hopes of understanding the mechanism of action.

  • Christian Randal Marks, BA

    Graduate Student, Colbran laboratory, Molecular Physiology & Biophysics

    Calcium/calmodulin-dependent kinase II (CaMKII) is a highly abundant serine/threonine kinase in the brain. Direct interactions between activated CaMKII and its substrates play a number of important roles within the cell such as feedback regulation of channels/receptors, and normal synaptic plasticity. Relatively few CaMKII-associated proteins are known to preferentially interact with inactive CaMKII, and their functional roles are poorly understood. Moreover, molecular mechanisms underlying the coupling of CaMKII to the G-protein coupled receptors (GPCRs) that stimulate the release of intracellular calcium are poorly characterized. An interaction between inactive CaMKII and the metabotropic glutamate receptor 5 (a Gq-coupled GPCR) was recently reported. I am currently investigating how CaMKII interactions with mGlu5 can change mGlu5 signaling. Understanding the physiological importance of this interaction may lead to novel treatments of neurological disorders linked to dysfunction of mGlu5 such as Parkinson’s Disease, addiction, schizophrenia, and autism spectrum disorder.

    724 Robinson Research Building

  • Sarah C. Milian

    Graduate Student, Jacobson laboratory, Molecular Physiology & Biophysics

    Our lab studies the function of potassium channels in electrically excitable endocrine cells within the pancreas. We are particularly interested in the β-cell specific potassium channel, TALK-1. TALK-1 is the most abundant potassium channel in the β-cell, and a polymorphism within TALK-1 has been associated with an increased risk for Type-2 diabetes. Our lab has previously shown that TALK-1 channels regulate the β-cells ability to release insulin in response to glucose. My work focuses on characterizing this regulation so that we can better understand the function that the channel plays in diabetes.

  • Kim Ramil Montaniel

    Graduate Student, Harrison laboratory, Molecular Physiology & Biophysics

    My research focus in the Harrison lab is on studying the role of reactive oxygen species in vascular function especially in the setting of hypertension and cardiovascular disease

  • Tyler L. Perfitt, BA

    Graduate Student, Colbran lab, Molecular Physiology & Biophysics

    Brain function relies on the formation and stabilization of synapses, and many neurological disorders are associated with disruptions in synaptic signaling. Scaffolding proteins play a critical role in maintaining spine morphology and bringing receptors and ion channels in close proximity to their downstream signaling molecules. In the Colbran lab, I study protein-protein interactions between CaMKII and scaffolds in the postsynaptic spines of neurons, and how they regulate downstream signaling. I am also interested in how neurons signal from the synapse to the nucleus in order to initiate gene transcription, an important process in learning and memory.

    BA, DePauw University

  • Diane Caitlin Saunders, BS, BA

    Graduate Student, Powers laboratory, Molecular Physiology & Biophysics

    In the Powers Lab, I am investigating the role of pancreatic endothelial cell populations in the islet microenvironment, by determining their role in macrophage recruitment and beta cell regeneration. I am also isolating subpopulations of human islet cells, ultimately characterizing how gene expression varies during developmental stages and in disease states.

    8435 MRB IV

  • Leslie Roteta Sedgeman, BA

    Graduate Student, Vickers laboratory, Molecular Physiology & Biophysics

    Communication by HDL-miRNAs in Type 2 Diabetes

    MicroRNAs (miRNAs) are small non-coding RNAs that post-transcriptionally repress gene expression and are found in both cells and extracellular fluids, including plasma. Extracellular miRNAs are protected from circulating nucleases through their association with lipid and protein carriers, specifically exosomes and lipoproteins.. Currently, I am studying the role of high-density lipoproteins (HDL)-miRNAs as cell-to-cell messengers in a novel endocrine-like communication pathway within Type 2 diabetes. We found that many of the most abundant miRNAs on HDL are also enriched in insulin-producing β-cells in the islets of Langerhans. Additionally, we found that the miRNA signature on HDL is significantly altered in rat models of Type 2 diabetes; therefore, the goal of my project is to investigate the molecular mechanisms by which the β-cell-originating miRNAs control gene expression in distal tissues and how this pathway regulates systemic lipid and glucose metabolism. Using high-throughput genomics, I aim to decode and control miRNA intercellular communication to better understand and treat type 2 diabetes, including developing biomarkers to predict pre-diabetes.

    358 RRB

  • Shannon Townsend

    Graduate Student, Gannon laboratory, Molecular Physiology & Biophysics

  • Elijah Trefts

    Graduate Student, Wasserman laboratory, Molecular Physiology & Biophysics

    Liver is a primary site of macronutrient metabolism. Obesity linked diseases of the liver such as nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) result in ECM expansion, defective hormonal responses, and disrupted transcriptional networks. Integrin receptors and their immediate post-receptor pathways convert sensory inputs from the ECM to biochemical processes within the cell. Altered expression of several integrin signaling components accompanies the metabolic dysregulation that occurs in high fat (HF)-fed mice. The mechanisms linking ECM expansion and integrin signaling to metabolic disease are a primary focus of our lab. My research utilizes hepatocyte specific knockout of several integrin signaling components (e.g. integrin α5, integrin β1, and Integrin-linked kinase) in mice to fully characterize these pathways and their involvement in pathologic responses of the liver to high fat feeding.

  • Rohit Venkat

    Graduate Student, Neuert Laboratory, Molecular Physiology & Biophysics

    In the Neuert Lab, I study long noncoding RNAs (lncRNAs), a class of non-protein coding transcripts that represents an emerging, previously unrecognized layer of gene regulation.  LncRNAs have been shown to mediate important biological processes ranging from cell cycle progression and cellular reprogramming to dosage compensation in mammalian development, but their mechanisms of action remain poorly understood. I work toward addressing these fundamental knowledge gaps.

  • John (Jack) Walker

    Graduate Student, Powers laboratory, Molecular Physiology & Biophysics

    My project focuses on defining the molecular signatures defining islet dysfunction in recent-onset type 2 diabetes in human tissues. To do this, I am characterizing the functional, morphologic, and transcriptional profiles of islets from individuals with type 2 diabetes using a combination of human pancreatic tissue, isolated islets, and sorted islet cell populations. I am also investigating the source of amyloid heterogeneity in type 2 diabetic islets.

  • Carrie Beth Wiese, BS

    Graduate Student, Vickers laboratory, Molecular Physiology & Biophysics

    Extracellular microRNAs have been identified in plasma, and our laboratory has identified these extracellular microRNAs are carried by lipoproteins including high-density lipoprotein (HDL). The goal of our laboratory is to characterize the role of these extracellular microRNAs, particularly to elucidate whether extracellular microRNAs may function as a novel cell-to-cell communication pathway. Within cells, microRNAs are small non-coding RNAs that post-transcriptionally regulate gene expression. Specifically, I study the myeloid-derived microRNA, miR-223, to understand to what tissue and cell types receive microRNA-223 after being exported from myeloid cells. To do this, I utilize bone marrow transplants between wild-type and miR-223 knockout mice to restore or deplete the myeloid (miR-223 donor cell) population. After restoring or depleting the myeloid population (miR-223 donor cell) I examine variety of tissue types and pure cell isolations to map out the delivery of extracellular miR-223 in vivo. My second project focuses on the role of endothelial microRNAs in the progression of Chronic Kidney Disease-associated atherosclerosis. I have found that complexing two microRNA inhibitors to HDL, allows me to effectively reduce endothelial microRNA levels. The decreased microRNA levels result in a dramatic reduction in atherosclerosis in vivo, which may be mediated through altered FAM220a regulation of STAT3 activation causing less inflammation.

    358 PRB

  • Ian Miller Williams, BS

    Graduate Student, Wasserman laboratory, Molecular Physiology & Biophysics

    Impaired insulin-stimulated muscle glucose uptake is a hallmark of insulin resistance and Type 2 diabetes. Before insulin can stimulate the muscle to take up glucose, it must first cross the endothelial barrier that separates the plasma from the interstitial fluid that bathes myocytes. I have developed an intravital microscopy technique which allows us to directly visualize and quantitate the trans-endothelial efflux of insulin in skeletal muscle. I am using this technique to 1) determine the mechanism by which insulin crosses the endothelium (i.e. receptor-mediated transport or passive diffusion) and 2) determine if impaired trans-endothelial movement of insulin may contribute to muscle insulin resistance.

    823 Light Hall