Kansas City Faculty Research
KCU's esteemed faculty conducts research in a variety of fields from molecular and cellular biology to infectious diseases and biomechanics. Each faculty member has years of experience in research and is available for partnerships and student mentorship.
A. Baki Agbas, MSc, PhD
Professor of Biosciences
Research Interests: Biomarkers for Neurodegenerative Diseases
- The Agbas’ lab is working on the development of a blood-based biomarkers for neurodegenerative diseases such as Alzheimer’s disease (AD) and Amyotrophic lateral sclerosis (ALS), also known Lou Gehrig’s disease. Our lab is collaborating with clinicians several clinical trials like Rasagilin-80 and oxaloacetate trial for ALS patients. Assessing the oxaloacetic acid (OAA) treatment for ALS model mouse as part of explorative study for developing treatment for human ALS. We published a peer-reviewed paper pertinent to this subject: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8155202/
- Mitochondrial respiration profile in Alzheimer’s disease and ALS as a potential biomarker. Currently, our lab is collaborating with KUMC researches to study on Functional Biomarkers for ALS. In this study, we are working on to validate serum mitochondrial and proteostasis biomarkers in ALS.
- Brain derived exosomes (i.e., neuronal derived exosomes (NDE), microglia derived exosomes (MDE), and astrocytes derived exosomes (ADE) are valuable venues to study blood –based biomarkers for neurodegenerative diseases. The goal of this study is to determine if circulating extracellular vesicles (EV) sub-organelles, micro vesicles (MV) and exosomes (EXO) may serve as a key pathway for clearance of pathological proteins that are relevant in amyotrophic lateral sclerosis (ALS) disease; hence, they may be identified as valid blood-based biomarkers. Absence of such biomarkers and the variability in clinical findings may make the diagnosis and prognosis of ALS disease difficult. To develop an assay strategy for determining the chemical modifications profile of signature proteins (i.e., tau and p-tau, pTDP-43, , TDP-43, SOD1, and FUS) is a valuable tool. This work is supported and funded by an intramural grant. We published a preprint paper pertinent to this subject: https://www.biorxiv.org/content/10.1101/2021.06.17.448876v2
- Dysfunctional proteolytic machinery in neurodegenerative diseases. Our lab along with very few other labs demonstrated that platelets could offer to study proteolytic machinery in human blood. To establish a human platelet-based autophagy assessment is innovative. In long run, this project will provide a real-time assessment for aberrant protein removal efficiency in AD upon treatment. The aberrant protein aggregation is a major issue in AD and only available assessment approach is to measure the aberrant protein levels; however, aberrant protein removal system assessment is equally important such as autophagy machinery. This approach will enhance the development and testing of new drugs for AD. Blood platelet-based autophagy assessment approach will provide a peripheral cell platform as an important biomolecular tool to design and implement clinical trials that testing the activation of autophagy machinery in AD. This project will incrementally move the field of blood-based biomarker development for AD. We published a peer-reviewed paper pertinent to this subject: https://jumdjournal.net/article/view/3342
Doug Bittel, MSc, PhD
Professor of Biosciences
Alternative splicing (AS) of mRNA plays an important role in development and pathogenesis. However, the mechanisms that regulate AS are poorly understood. Our studies of gene processing in heart tissue from babies with congenital heart defects suggests that a family of small noncoding RNA, scaRNAs, adjust alternative splicing through biochemical modification of the spliceosome. Our studies suggest that when scaRNAs do not function adequately it leads to inappropriate mRNA splicing that contributes to congenital heart defects. Our observations, using human cell cultures clearly show that altering the expression level of scaRNAs alters mRNA splicing. Furthermore, using zebrafish and quail embryos, we have shown that altering scaRNA expression levels in the embryo alters mRNA splicing and embryonic development. We hypothesize that scaRNAs play an important role in regulating development and when they are dysregulated, they contribute to developmental pathology. This is a new paradigm in developmental regulation; therefore, it is important that we develop a better understanding of the role that scaRNAs play in alternative splicing of mRNA and development.
We are also collaborating with a biotech company, Likarda, in developing a stem cell-based cure for Type 1 diabetes. In phase 1, Likarda is inducing pluripotent stem cells to differentiate into insulin-producing cells. They will transplant these cells into companion animals. Our role is to evaluate multiple biomarkers as the cells differentiate to ensure that the process is proceeding as expected. Their business model is to do clinical trials in companion animals to demonstrate proof of concept prior to adapting the process for human application.
Nicole Ford, PhD
Assistant Professor of Biosciences
Evolution and disease are both driven by DNA mutations. Certain small molecules can cause DNA damage by inserting themselves between and forming covalent adducts with neighboring DNA base pairs. Cells view these adducts as DNA damage, and DNA damage repair enzymes have an inherently low replication fidelity. Therefore, repair of the damage from intercalating chemicals often results in residual DNA mutation. Additionally, these chemicals follow specific rules for intercalation location and productive adduct formation. Yet these rules are not fully elucidated despite decades, if not centuries, of use and/or exposure to these chemicals. For example, medicinal uses of Psoralens have been reported for millennia, and 8-methoxypsoralen currently is used in conjunction with UVA light (PUVA treatment) for many dermatological ailments. Understanding whether specific gene sequences could be targeted and subsequently mutated due to psoralen photoadduct formation would help to predict long-term side effects of these treatments. In addition to Psoralens, some other interesting examples of intercalating chemicals are: DNA alkylating agents used as cancer chemotherapeutics (e.g., mitomycin C and daunomycin ), or the mutagenic agents from automobile exhaust (nitropyrenes) and cigarette smoke (benzo[a]pyrene diol epoxides).
The central goal of this research is to create a scalable, modular, and affordable system for the production of biosilica materials that have been functionalized with a biosensor that detects a medically relevant agent. Diatoms are a group of unicellular microalgae, often with a highly silicified, mesoporous cell wall (frustule). The species used in this research is Thalassiosira pseudonana, a model organism for in vivo self-assembly of genetically-modified frustules. The biosensors are constructed by creating a fusion protein containing a silica-targeting peptide and the biosensor (synthetic antibody) against the desired pathogen that is driven by a diatom-specific promoter. Recently, an improved method of inserting DNA into diatoms was published: conjugation with bacteria. Due to the small number of researchers who use diatoms for genetic engineering, this method is only being performed in 2-3 labs worldwide! Once diatoms are engineered to express the biosensor protein in their porous frustules, the cultures could be scaled up to industrial levels – thereby creating an affordable source of biosensors immobilized in silica.
Eugene Konorev, MD, PhD
Associate Professor of Pharmacology
Research Interests: Angiogenesis and Cardiovascular Complications of Anticancer Therapy
Utilizing animal models and cell culture, Dr. Konorev’s research is focused on the prevention of cardiac remodeling and progression of heart failure resulting from cancer chemotherapeutics. His team has made important contributions to the field of angiogenesis or the process of formation of new vascular networks in postnatal tissues. He has identified targets for the antiangiogenic effect of doxorubicin and therapeutics to alleviate the antiangiogenic effects.
Józia (Jozi) McGowan, DO, FACOI, FNAOME, CS
Associate Professor of Internal Medicine
Director of COM Student Success
Research Interests: Resiliency, Emotional Intelligence, Medical School Clinical Education
Józia (Jozi) McGowan, DO, FACOI, FNAOME, CS is a board-certified Internal Medicine Physician. She graduated from Kansas City University, KCU-COM (KC, MO), in 2009 and did her Internal Medicine residency in Michigan. After practicing outpatient Internal Medicine, she entered into academic medicine and has been faculty for her alma mater, since 2015. As part of the clinical teaching faculty, she is involved in educating, mentoring, and advising students from all four years of medical school. In 2016, she became a part of the administrative team as the Curriculum Phase II Director- KC; heavily involved in the curriculum and success of the second-year medical student cohort. On July 1, 2021, Dr. McGowan’s administrative role transitioned to Director of COM Student Success, which helps her focus even more on living out KCU’s vision. She is a Fellow in the American College of Osteopathic Internists (FACOI), a Fellow of the American Association of Colleges of Osteopathic Medicine’s National Academy of Osteopathic Medical Educators (FNAOME) in the category of Teaching and Evaluation, and a Costin Scholar (CS): Midwestern University’s, The Costin Institute for Osteopathic Medical Educators. Dr. McGowan is passionate about medical education and student wellness and success. She has received the Advocate for Academic Excellence award and was inducted into and is currently chapter advisor of The Gold Humanism Honor Society at KCU.
Ehab Sarsour, MSc, PhD
Assistant Professor of Cellular and Molecular Biology
Research Interest: Aging and age-associated diseases including cancer
Dr. Sarsour's research interests focus on the molecular mechanisms that regulate the proliferative properties of normal and cancer cells. Dr. Sarsour proposed that two separate, but interdependent pathways could regulate cellular longevity in normal cells: a redox-sensitive checkpoint regulating the transition from quiescence to proliferation also known as chronological life span followed by telomeric attrition controlling the “mitotic clock” known as replicative life span. My research has shown that the antioxidant enzyme manganese superoxide dismutase protects quiescent normal human fibroblast regenerative capacity (chronological life span) by regulating mitochondrial reactive oxygen species and protecting mitochondrial integrity from age-associated abnormalities. Dr. Sarsour's work has evolved into examining the molecular mechanisms associated with oxidative stress and metabolic alteration during cellular aging and its effects on cancer progression. The scope of his current and future work is to understand how cellular redox status, reactive oxygen species, and lipid metabolism regulate cellular aging in human tissue and their effect on the microenvironment of diseased tissue, with the goal of enhancing the human health life span. Dr. Sarsour is also working on different translational research strategies that relate to manipulating the cancer microenvironment to enhance chemo and radiotherapies to achieve a better outcome for cancer patients.
Robert White, PhD
Dean of the College of Biosciences, Professor of Molecular Biology and Medical Genetics
Duchenne Muscular Dystrophy (DMD)
Dr. White's lab has been developing a novel therapy to treat Duchenne Muscular Dystrophy (DMD), a lethal muscle degeneration disease commonly found in boys for which there is no cure and is caused by the lack of a muscle protein called dystrophin. Expression of a protein from the eye (retinal dystrophin) in DMD model mice by a transgene cures the mice of their disease which includes severe muscle degeneration accompanied by loss of limb movement and early death. Dr. White's next goal is to move from the lab bench to the bedside of patients. He and his team are identifying the promoter of the retinal dystrophin as a first step in identifying drugs which will induce its expression in muscle. The genetic machinery to make eye dystrophin in muscle is present in many DMD patients but is not used because it is not retinal tissue. Their long-range goal is to find drug(s) that induce expression of eye dystrophin from its promoter in muscle as a cure for DMD.
Hematological Diseases Project 1
Iron overloading is a debilitating disease that can occur in a genetic disease (Hereditary Hemochromatosis) or in blood transfusion-dependent diseases such as beta-thalassemia and sickle cell disease. Iron overloading can lead to heart, kidney and pancreatic disease which presents as severe morbidity. The treatment for this disease is using iron-chelating drugs for which patient compliance is low. Hemochromatosis patients are treated by bloodletting as this is the only method by which treatment can remove iron from the body. Dr. White's lab has a mouse mutant that excretes 100x more iron in urine and, when mated to hemochromatosis model mice, can prevent iron overloading. His study is to identify the mechanism and pharmaceutical targets to induce this urinary iron excretion to treat patients with iron overload.
Hematological Diseases Project 2
In a second project, Dr. White's lab is in the process of identifying a novel erythroid transcription factor to treat anemia and potentially identify a novel treatment for leukemia. This work derives from the study of an interesting mouse mutant (call Xpna: x-linked pre and neonatal anemia) which lacks the most important erythroid transcription factor called GATA1. The mice with a GATA1 mutation are born anemia but unexpectedly receiver from their anemia. The hypothesis being tested is that there is a compensatory erythroid transcription factor that replaces GATA1 in these mice and also has the likely characteristic that it can prevent leukemia as well.
Barth Wright, PhD
Associate Professor of Anatomy
Research Interests: Comparative Anatomy and Behavior
Dr. Wright's research examines the various interactions among human and non-human primate food mechanics behavior and morphological and physiological adaptations, particularly craniofacial. These tools and techniques include, but are not limited to, detailed in-field observations of feeding in field tests of food mechanical properties combined with laboratory measures of force transduction using high fidelity 3D imaging and force measurement. His research incorporates a range of tools and techniques, the use of which can prove beneficial to evolutionary biologists and clinicians.
Asma Zaidi, PhD
Professor of Biochemistry
Research Interests: Neurobiology of Brain Aging and Neurodegenerative Disorders
Teaching Expertise: Basic and Clinical Biochemistry, Molecular and Cell Biology
Dr. Zaidi’s research interests are focused on investigating the mechanisms underlying neuronal cell death in brain aging and in neurodegenerative disorders. Her work has shown that disruption of calcium homeostasis is the final common pathway leading to the death of neurons in the central nervous system. She focuses on a calcium transporter called the plasma membrane Ca2+-ATPase (PMCA). The PMCA is responsible for pumping calcium out of neurons to maintain a 10,000-fold gradient that exists across the plasma membrane and is critical for optimal functioning of neurons. Her research showed for the first time that the activity and protein levels of PMCA are progressively reduced in the brain with increasing age. She has also shown that this protein is extremely sensitive to oxidative stress and undergoes inactivation, aggregation and proteolysis when exposed to reactive oxygen species of physiological relevance.
Dr. Zaidi’s recent work has identified that the PMCA plays an important role in the selective degeneration of dopaminergic neurons in Parkinson’s Disease (PD). Utilizing human brain post-mortem tissue animal model as well as a cell culture model of PD, she showed that endogenous levels of PMCA are lower in the substantia nigra of the brain compared to other regions. Additionally, PMCA activity is significantly reduced when exposed to PD mimetics. Currently, she is developing novel strategies to increase the expression of the PMCA, which may serve as a translational target for therapeutic intervention in PD. Several antioxidant flavonoid compounds including resveratrol, curcumin, fisetin and edaravone are emerging as promising targets.