Prof. Dr. Peter Koulen
Departments of Ophthalmology and Basic Medical Science, School of Medicine, University of Missouri - Kansas City, 2411 Holmes Street, Kansas City, MO 64108, USA
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Academic Career Length
19Years (2008-Present)
(Calculated once Scilit publication data is synced: current year − year of first publication + 1)
Representative Publications
View All Publications2 May 2017 in Current Protocols in Toxicology
Journal Article
SKSimon Kaja
Simon Kaja
APAndrew J. Payne
Andrew J. Payne
YNYuliya Naumchuk
Yuliya Naumchuk
Peter KoulenDrug discovery heavily relies on cell viability studies to assess the potential toxicity of drug candidates. L‐Lactate dehydrogenase (LDH) is a cytoplasmic enzyme that catalyzes the concomitant interconversions of pyruvate to L‐lactate and NADH to NAD+ during glycolysis, and the reverse reactions during the Cori cycle. In response to cellular damage, induced by endogenous cellular mechanisms or as a result of exogenously applied insults, LDH is released from the cytoplasm into the extracellular environment. Its stability in cell culture medium makes it a well‐suited correlate for the presence of damage and toxicity in tissues and cells. We herein present protocols for a reproducible and validated LDH assay optimized for several cell types. In contrast to commercially available LDH assays, often associated with proprietary formulations and high cost, our protocols provide ample opportunities for experiment‐specific optimization with low variability and cost. © 2017 by John Wiley & Sons, Inc.
Journal Article
The significance of oxidative stress in the development of chronic neurodegenerative diseases of the retina has become increasingly apparent in recent years. Reactive oxygen species (ROS) are free radicals produced at low levels as a result of normal cellular metabolism that are ultimately metabolized and detoxified by endogenous and exogenous mechanisms. In the presence of oxidative cellular stress, ROS are produced in excess, resulting in cellular injury and death and ultimately leading to tissue and organ dysfunction. Recent studies have investigated the role of excess ROS in the pathogenesis and development of chronic neurodegenerative diseases of the retina including glaucoma, diabetic retinopathy, and age-related macular degeneration. Findings from these studies are promising insofar as they provide clear rationales for innovative treatment and prevention strategies of these prevalent and disabling diseases where currently therapeutic options are limited. Here, we briefly outline recent developments that have contributed to our understanding of the role of ROS in the pathogenesis of chronic neurodegenerative diseases of the retina. We then examine and analyze the peer-reviewed evidence in support of ROS as targets for therapy development in the area of chronic neurodegeneration of the retina.
22 March 2021 in Frontiers in Endocrinology
Journal Article
HRHussain Rao
Hussain Rao
JJJonathan A. Jalali
Jonathan A. Jalali
TJThomas P. Johnston
Thomas P. Johnston
Peter KoulenDiabetic retinopathy (DR) is a significant cause of vision loss and a research subject that is constantly being explored for new mechanisms of damage and potential therapeutic options. There are many mechanisms and pathways that provide numerous options for therapeutic interventions to halt disease progression. The purpose of the present literature review is to explore both basic science research and clinical research for proposed mechanisms of damage in diabetic retinopathy to understand the role of triglyceride and cholesterol dysmetabolism in DR progression. This review delineates mechanisms of damage secondary to triglyceride and cholesterol dysmetabolism vs. mechanisms secondary to diabetes to add clarity to the pathogenesis behind each proposed mechanism. We then analyze mechanisms utilized by both triglyceride and cholesterol dysmetabolism and diabetes to elucidate the synergistic, additive, and common mechanisms of damage in diabetic retinopathy. Gathering this research adds clarity to the role dyslipidemia has in DR and an evaluation of the current peer-reviewed basic science and clinical evidence provides a basis to discern new potential therapeutic targets.
Journal Article
AMAudrey E. McCalley
Audrey E. McCalleySKSimon Kaja
Simon KajaAPAndrew J. Payne
Andrew J. PaynePeter KoulenResveratrol is a naturally occurring compound contributing to cellular defense mechanisms in plants. Its use as a nutritional component and/or supplement in a number of diseases, disorders, and syndromes such as chronic diseases of the central nervous system, cancer, inflammatory diseases, diabetes, and cardiovascular diseases has prompted great interest in the underlying molecular mechanisms of action. The present review focuses on resveratrol, specifically its isomer trans-resveratrol, and its effects on intracellular calcium signaling mechanisms. As resveratrol’s mechanisms of action are likely pleiotropic, its effects and interactions with key signaling proteins controlling cellular calcium homeostasis are reviewed and discussed. The clinical relevance of resveratrol’s actions on excitable cells, transformed or cancer cells, immune cells and retinal pigment epithelial cells are contrasted with a review of the molecular mechanisms affecting calcium signaling proteins on the plasma membrane, cytoplasm, endoplasmic reticulum, and mitochondria. The present review emphasizes the correlation between molecular mechanisms of action that have recently been identified for resveratrol and their clinical implications.
Journal Article
APAndrew J. Payne
Andrew J. PayneSKSimon Kaja
Simon KajaYNYuliya Naumchuk
Yuliya NaumchukNKNancy Kunjukunju
Nancy KunjukunjuPeter KoulenThe molecular pathways contributing to visual signal transduction in the retina generate a high energy demand that has functional and structural consequences such as vascularization and high metabolic rates contributing to oxidative stress. Multiple signaling cascades are involved to actively regulate the redox state of the retina. Age-related processes increase the oxidative load, resulting in chronically elevated levels of oxidative stress and reactive oxygen species, which in the retina ultimately result in pathologies such as glaucoma or age-related macular degeneration, as well as the neuropathic complications of diabetes in the eye. Specifically, oxidative stress results in deleterious changes to the retina through dysregulation of its intracellular physiology, ultimately leading to neurodegenerative and potentially also vascular dysfunction. Herein we will review the evidence for oxidative stress-induced contributions to each of the three major ocular pathologies, glaucoma, age-related macular degeneration, and diabetic retinopathy. The premise for neuroprotective strategies for these ocular disorders will be discussed in the context of recent clinical and preclinical research pursuing novel therapy development approaches.
Journal Article
RDRaymond Scott Duncan
Raymond Scott DuncanDGDaryl L. Goad
Daryl L. GoadMGMichael A. Grillo
Michael A. GrilloSKSimon Kaja
Simon KajaAPAndrew J. Payne
Andrew J. PaynePeter KoulenBoth acute and chronic degenerative diseases of the nervous system reduce the viability and function of neurons through changes in intracellular calcium signaling. In particular, pathological increases in the intracellular calcium concentration promote such pathogenesis. Disease involvement of numerous regulators of intracellular calcium signaling located on the plasma membrane and intracellular organelles has been documented. Diverse groups of chemical compounds targeting ion channels, G-protein coupled receptors, pumps and enzymes have been identified as potential neuroprotectants. The present review summarizes the discovery, mechanisms and biological activity of neuroprotective molecules targeting proteins that control intracellular calcium signaling to preserve or restore structure and function of the nervous system. Disease relevance, clinical applications and new technologies for the identification of such molecules are being discussed.
About Me
Prof. Dr. Peter Koulen is a Professor of Ophthalmology and
Biomedical Sciences, and the Felix and Carmen Sabates Missouri Endowed Chair in
Vision Research, at the UMKC School of Medicine. He trained at the Max-Planck
Institute for Brain Research, Yale University, and the Marine Biological
Laboratory. His research focuses on basic research and therapy development for
chronic diseases of the eye and brain. He is an internationally recognized
expert in biophysics, biochemistry, and physiology of nerve cells, and his
research has been funded continually since 2002 by national and international
foundations and agencies including the NIH’s National Eye Institute, National
Institute on Aging, National Cancer Institute, National Center for Research
Resources, National Institute of Diabetes and Digestive and Kidney Diseases,
and the U.S. DOD among others. He is a review panel member for several national
and international funding agencies including the National Science Foundation,
the National Institutes of Health, the U.S. Department of Defense, and other
national and international government agencies and research foundations. The
University of Missouri–Kansas City Board of Trustees recognized Dr. Koulen with
the N.T. Veatch Award for Distinguished Research and Creativity. Through this
Faculty Award, the UMKC and the UMKC Trustees recognize the very best
faculty members, who have distinguished themselves through scholarship and
creativity.