Our Research
Researchers within this area have expertise in studying the GI tract and liver, including bile acid, glucose, lipid and lipoprotein metabolism and GI mucosal biology.
Marc Basson, M.D., Ph.D., M.B.A.
Dr. Basson’s laboratory interests focus on the development of FAK-activating small molecules toward drugs to promote mucosal repair and on the role of SLFN12 in cancer biology. This work includes both cell culture studies and mouse and rat models. He also has extensive clinical research interests in surgical disease and the effects of blood pressure variability on health outcomes.
Jessica Ferrell, Ph.D.
Dr. Ferrell is interested in bile acid metabolism within the context of metabolic liver disease, which is growing in prevalence in the United States and globally. Bile acids are physiological detergents that also regulate glucose, cholesterol, and lipid homeostasis in the liver, gut, brain, and other tissues by binding to receptors. This liver-gut-brain axis ensures the liver adapts appropriately to changes in nutrient status and time of day as well as pathological stimuli. Chronic pathological insults (like diet, dysbiosis, alcohol, or circadian disruption) can result in metabolic dysfunction-associated steatotic liver disease or hepatitis (MASLD/MASH), dyslipidemia, Type II diabetes, and obesity. In turn, these disorders affect bile acid physiology and can worsen disease. The lab’s long-term research goals are to study 1) how metabolic liver disease disrupts bile acid metabolism, and 2) how bile acid signaling can be exploited as a therapeutic target for MASLD/MASH.
Takhar Kasumov, Ph.D.
Dr. Kasumov’s research has been focused on developing new high-throughput mass spectrometry-based technologies to understand dysregulated lipid, glucose and protein metabolism in obesity-associated diseases, including type 2 diabetes mellitus (T2DM) and non-alcoholic fatty liver disease (NAFLD) and their cardiovascular complications. We use different systems biology approaches coupled with biochemical and molecular techniques to elucidate the mechanisms of disrupted glucose, lipid and protein homeostasis, in the hope of uncovering novel therapeutic approaches.
Yoon-Kwang Lee, Ph.D.
Dr. Lee’s laboratory investigates the underlying molecular mechanisms of obesity and how they are related to metabolic disorders such as diabetes and fatty liver disease, which are pandemic in modern society due to high caloric intake and sedentary lifestyle. They focus on the group of proteins playing critical roles in bile acid and lipid synthesis pathways. Dr. Lee uses mouse models deficient in each of these proteins, which are strongly reminiscent of these disorders. The molecular and biochemical assessment of these models will help to understand the development of metabolic disorders and provide therapeutic or preventative approaches to halt their progression.
GUIMING LIU
Dr. Liu’s research focuses on three major areas: (1) the examination of urological complications associated with obesity and diabetes, with the goal of elucidating the pathophysiological mechanisms linking these metabolic disorders to bladder dysfunction, urinary incontinence, erectile dysfunction, and urinary tract infections; (2) the investigation of the pathogenesis of lower urinary tract dysfunction, with an emphasis on elucidating underlying mechanisms using preclinical animal models, particularly in bladder dysfunction, interstitial cystitis, and urinary incontinence; and (3) the exploration of gastrointestinal mucosal injury through the investigation of its molecular mechanisms and the development of novel therapeutic strategies for its prevention and treatment.
Priya Raman, Ph.D.
Dr. Raman’s laboratory studies vascular complications associated with diabetes, obesity and metabolic syndrome (MetS). In particular, our laboratory is interested in the role of ‘non-lipid factors’ such as thrombospondin-1 (TSP-1, a matricellular protein) and O-linked N-acetylglucosamine signaling (O-GlcNAc, a post-translational protein modification) in the pathogenesis of macrovascular disorders associated with diabetes and metabolic syndrome. We are specifically interrogating the cellular and molecular mechanisms by which TSP-1 and O-GlcNAc signaling regulate transition of VSMC and macrophages to atherogenic and inflammatory phenotypes, triggering augmented atherosclerotic complications in diabetes and MetS. We utilize a variety of biochemical, histological and molecular biology approaches in combination with en-face atherosclerotic lesion assay, non-invasive high-frequency ultrasound imaging, EchoMRI and CLAMS studies. In addition, we use human and mouse cell culture models in conjunction with in vivo mouse models of diabetes, obesity and atherosclerosis, including both conventional and inducible tissue-specific knockout mice.
Jaclyn Welles, Ph.D.
Dr. Welles’s research focuses on the mechanisms that facilitate the transition from a steatotic liver (metabolic dysfunction-associated steatotic liver disease, or MASLD) to a fibrotic liver (metabolic dysfunction-associated steatotic hepatitis, or MASH). This research examines how hepatic copper trafficking and utilization, alongside copper-dependent alterations in lipid profiles, such as glycosphingolipids, affect the activation of pro-fibrogenic hepatic stellate cells. Dr. Welles’ research also leverages advanced methodologies such as Single-Nuclei RNA-Seq, along with traditional and spatial proteomics, metallomics, and lipidomics, to delve deeper into the mechanisms driving fibrogenesis in the liver. The overarching goal of these studies is to identify novel, copper-regulatory pathways in cell-type specific populations enriched in the liver, to aid in the development of targeted therapeutics against MASH-associated fibrosis and inflammation.
Jianguo Wu, M.D., Ph.D.
Dr. Wu’s research program integrates genetically engineered mouse models, multi-omics approaches, molecular and cellular biology, biochemistry, genomics, and bioinformatics to investigate the molecular mechanisms underlying alcohol-associated liver disease (ALD), metabolic dysfunction–associated steatotic liver disease (MASLD), and cholestatic liver disease. His laboratory focuses on defining the metabolic regulation of hepatic stellate cell activation, elucidating the roles of non-coding RNAs in liver disease pathogenesis, and characterizing the interplay between cell death pathways and innate immune activation in liver injury and fibrosis. The long-term objective of this work is to delineate how dysregulated genes, signaling pathways, and molecular networks drive liver cell dysfunction and disease progression, and to identify novel biomarkers and therapeutic targets for the diagnosis, treatment, and prognosis of liver disease.
CONTACT
Jessica Ferrell, Ph.D.
Assistant Professor of Biomedical Sciences
jfrancl@neomed.edu
Phone: 330-325-6468
Office: F-242