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Funai Lab Photo

The Funai Lab
(9/22/14)The Funai Lab studies cellular processes by which skeletal muscle handles substrate overload during metabolic stress. As skeletal muscle is an organ with the highest metabolic demand, metabolic changes that occur in skeletal muscle have tremendous consequences on whole-body metabolism. Specifically, we are interested in the cellular fate of lipid molecules in skeletal muscle. We utilize cell lines, genetically-modified mice and biopsies from human subjects to examine mechanisms whereby skeletal muscles develop and/or evade toxic effects of lipid influx.

neufer lab - website

The Neufer Lab
(9/12/14)The Neufer Lab centers around mitochondria. Their research is directed at deciphering the molecular mechanisms governing mitochondrial bioenergetics and function in the context of the etiology of metabolic disease as well as disease prevention/treatment.

Huang lab - website

The Huang Lab
(9/08/14)The Huang Lab is currently focusing on answering the following scientific questions: 1)whether exercise induces hypothalamic neurogenesis and 2) which particular neurons in the hypothalamus controls moving behavior. Their plan is to open a new research avenue combining the various neuroscience techniques used on transgenic animal models to determine whole body metabolism with exercise and /or nutrition intervention.

Shaikh lab - website

The Shaikh Lab
(8/26/14)The Shaikh lab currently has three major projects . 1) The first project is trying to understand how omega-3 fatty acids, modeling pharmacological intake, serve to boost B cell mediated immunity in diet-induced obesity. Obese individuals display poor responses to vaccinations and infections and therefore there is a need to develop therapeutics to enhance immunity in these individuals. We have discovered that clinical grade omega-3 fatty acids can boost the antibody response to several antigens including in response to influenza infection. We are currently trying to understand the underlying mechanisms by which omega-3 fatty acids boost B cell responses. Our focus is on specialized pro-resolving mediators and the biophysical organization of the B cell plasma membrane. This work is in collaboration with Melinda Beck at UNC-CH. 2) The second project entails trying to understand how changes in cardiolipin levels in response to differing metabolic diseases dysregulate the formation, size, and stability of cardiolipin microdomains and thereby protein clustering in the inner mitochondria membrane of cardiomyocytes. Here we are using FRET and FRAP approaches coupled with enzymatic assays and functional studies in collaboration with the Zeczycki and Brown labs. 3) The third project is a deviation from our central focus on lipids. Here we are trying to understand how SAMe, a dietary supplement, suppresses pro-inflammatory cytokine secretion in primary macrophages. Our ultimate goal here is to link how changes in the inflammatory environment with SAMe impact the progression of depression in humans, where SAMe is known to exert beneficial effects.

Hickner lab - website

The Hickner Lab
(8/13/14)The Hickner Lab investigates areas of obesity, aging, exercise, nutrition, microvascular blood flow and lipolysis in skeletal muscle and adipose tissue. The areas of study have been diverse, encompassing exercise training and nutritional interventions across the lifespan, from prepubescent children to aged individuals. The studies have focused primarily on the regulation of microcirculation and lipolysis by nitric oxide and other compounds as studied with microdialysis and tissue biopsies in humans. Current funding in the Hickner lab supports studies into the effects of obesity, exercise training and nutritional intervention on reactive oxygen species and the regulation of nitric oxide synthase mediated skeletal muscle blood flow.

Zeczycki Lab - website

The Zeczycki Lab
(8/05/14)The Zeczycki Lab’s focuses on determining the mechanisms of catalysis and unraveling the complexities of allosteric regulation of those multifunctional enzymes that are important to the pathogenesis of disease states. Understanding the activity and regulation of these enzymes is critical for the development of effective therapeutics which can modulate, rather than inhibit, enzyme activity. The current focus of research in our lab is directed towards two different enzymes, pyruvate carboxylase (PC) and transglutaminase 2 (TG2). The aberrant activities of these enzymes are partially responsible for the pathogenesis and exacerbation of Type 2 diabetes and neurodegenerative diseases, respectively. In order to determine the physiologically relevant kinetic, chemical and allosteric mechanisms inherent to these enzymes, our lab uses a combination of in vitro techniques to examine the unique enzymatic biochemical transformations, dynamic domain motions and inter-subunit communication pathways. These techniques, common to the fields of molecular biology, chemical biology and enzymology, include protein engineering, site-directed mutagenesis, steady-state and pre-steady-state kinetics and 1D/2D NMR.

houmard lab - website

The Houmard Lab
(7/30/14)The Houmard Lab’s primary focus is examining how skeletal muscle metabolism is altered with conditions such as obesity, type 2 diabetes and the aging process, and how a physically active lifestyle can counteract decrements associated with these conditions. Current ongoing projects involve how fat oxidation is altered with obesity, the role of exosomes in the insulin resistance of obesity, the metabolic changes seen with gastric bypass surgery, and how exercise training can rescue the reduction in fat oxidation and insulin resistance seen with obesity.

mcclung lab - website

The McClung Lab
(7/25/14)The McClung Lab is focused on understanding the molecular mechanisms of angiogenesis and vascular remodeling in both physiologic and pathologic processes, including: exercise, peripheral artery disease (PAD), atherosclerosis, cardiac and cerebral ischemia, diabetes, and cancer. The lab is interested in how genetic variation may direct the integration of individual cellular responses to ischemic insult, resulting in differential manifestations of tissue pathology in both pre-clinical models and in clinical patient populations. On a deeper level, the lab is studying how single nucleotide polymorphisms affect autophagy, mitochondria, oxidative stress, and signal transduction by endothelial receptor tyrosine kinase (RTKs) in different cell types (skeletal muscle, endothelial, progenitor, smooth muscle, fibroblast). Therapeutic strategies targeting the vasculature in cardiovascular disease have met with little success, and those aimed at preventing tumor angiogenesis result in significant side effects that often result in forced cessation of therapy. The McClung lab hopes to lay the foundation for the development of novel diagnostic and therapeutic tools for tissue ischemia and aid in the refinement of current anti-angiogenic therapies for cancer. The lab currently consists of Dr. McClung (PI), Cameron Schmidt (Graduate Student). Tom Green (currently in Oncology as a Research Associate) will be joining the lab August 1.

brown lab - website

The Brown Lab
(7/16/14)The DB Laboratory is interested in developing new therapies for heart disease. The heart is the most metabolically active organ in the body, and our experiments seek to determine how the mitochondrial network sustains the energy supply necessary to support cardiac electromechanical function. During many pathological states, such as diabetes or following a heart attack, mitochondria don’t “breathe” as well as they do in the healthy state. We want to know what goes wrong, and if there are interventions that can improve heart function by targeting mitochondria. In particular, we study the effects of exercise and mitochondria-targeting therapeutics on cardiac function during conditions where energetics are impaired. For the last 5 years, we have been working with a series of cell-permeable peptides that localize to mitochondria. These peptides can lower mitochondrial production of reactive oxygen species, and keep the mitochondrial “energy grid” operational. We are currently studying how these peptides interact with cardiolipin – a phospholipid in the inner mitochondrial membrane that influences the temporal/spatial organization of the electron transport system. One of these peptides, MTP-131 (Bendavia), is currently being tested in two different clinical trials for heart disease. In addition to his ECU duties, Dr. Brown works as an advisor for Stealth Peptides, the company that is developing many of the peptides.

cabot lab - website

The Cabot Lab
(7/9/14)The Cabot Lab focuses on sphingolipid metabolism as it relates to cancer growth and therapy. Sphingolipid metabolism is an area of cancer research that has risen to clinical prominence over the last 15 years. This is because ceramide, the aliphatic backbone of sphingolipids, acts as a powerful tumor suppressor, whereas its glycosylated product, glucosylceramide, catalyzed by the enzyme glucosylceramide synthase, is anti-apoptotic and a biomarker of multidrug resistance, as identified by Cabot in the mid-1990’s. Acid ceramidase, another important sphingolipid enzyme regulator of cancer cell growth, has recently been identified as candidate gene for development of new cancer diagnostics and touted as a therapeutic target in metastatic cancer. Like glucosylceramide synthase, acid ceramidase dampens the tumor suppressor properties of ceramide via ceramide hydrolysis and leads to the generation of sphingosine 1-phosphate, a powerful cancer cell mitogen. Thus, sphingolipid metabolism is a dynamic process with complex orchestration, impact, and clinical applications. Importantly, these enzymes are druggable targets.
geyer lab - website
The Geyer Lab
(7/1/14)The Geyer lab is interested in how retinoic acid (RA) directs the initial steps of male germ cell development. RA regulates the sex-specific timing of meiotic initiation in mice, which in males occurs at postnatal day (P)10. However, RA signaling initiates 1 week prior, at P3-4, yet we know almost nothing about the pathways or mechanisms initiated by RA signaling and their relationship to neonatal male germ cell differentiation. We recently discovered that RA directs neonatal germ cell proliferation, ultrastructure maturation (mitochondria and Golgi biogenesis), modified timing of meiotic initiation, and the expression of differentiation markers such as STRA8 and KIT. In addition, we found that RA stimulates translation of a panel of mRNAs in differentiating spermatogonia, and this discovery is the current focus of investigations in the Geyer laboratory. We are currently using in vivo and ex vivo approaches with neonatal testis explants in combination with RA and a variety of inhibitors to understand how RA signaling enhances the translation of mRNAs encoding critical differentiation markers such as STRA8 and KIT. The identification of pathways activated by RA will provide a significant advance in our understanding of how cell fate decisions are made at the initiation of spermatogenesis and provide insight into the etiology of testicular cancers and male infertility.
bridges - website
The Bridges Lab
(6/25/14)The Bridges Lab is specifically interested in how Vitamin A (retinol) oxidative metabolites alter immune cell adhesion. Although the requirement of vitamin A in immunity has long been appreciated, only within the past three decades have the molecular mechanisms by which retinoids elicit their effects been elucidated. We are currently using various molecular and cellular tools to investigate the impact of retinoids on the action of a special family of proteases known as ADAMs (a disintegrin and metalloprotease). Since ADAMs are novel proteases that can also serve as cell substrates for adhesion, we posit that retinoid exposure and ADAM function interplay during immune cell trafficking.