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School of Medicine Greenville


Faculty Profile

Faculty and Staff

Richard Lance Goodwin, Ph.D.

Title: Associate Professor
Biomedical Sciences
School of Medicine Greenville
E-mail: goodwirl@greenvillemed.sc.edu
Phone: 864-455-7476
   
Office: 607 Grove Road
Greenville SC
profile

Bio

Background: Since completing my postdoctoral training with Dr. David Bader, I have established a research program that investigates mechanisms of embryonic development and disease. My lab has generated in vitro 3D models of different aspects of cardiac development including myocardial, valve and coronary vessel development. This work has resulted in numerous publications and has been supported by funding from NIH, NSF, Biotech Research Partnerships, and Private Foundations. These studies have led to an interest in the development of fibrous tissues, which occurs normally during embryonic development and pathologically in a number of disease processes.
Teaching Interest(s): Medical Embryology Medical Histology Anatomy Developmental Biology and Regeneration Cardiovascular Developmemt
Research Interest(s): My work has been to investigate the mechanisms of cardiovascular development. The importance of this work is two fold. First, cardiovascular malformations are the most common birth defects. Elucidation of developmental mechanisms provides opportunities for new therapies for these deadly and debilitating disorders. Second, new cell-based therapies to treat adult disorders are likely to use these same developmental mechanisms to regenerate malformed and diseased structures. As my training dictated, my initial approaches were largely genetic in nature. That is, I focused on dissecting the genetic pathways that regulate cardiovascular development. While this approach remains a critical part of my research strategy, results from key experiments indicated that the mechanical environment has a profound effect on genomic regulation of the differentiation and morphogenesis of cardiovascular tissues. Indeed, a large body of clinical and experimental evidence supports these findings. Together these data have led to my view that, with the correct cellular and mechanical milieu, any cardiovascular structure could be generated or regenerated. The cellular components are fairly well established; however, there is a great deal to be discovered concerning the mechanical environment. For this reason, I have moved my research more toward bioengineering approaches. I believe, working with my collaborators at Clemson, will allow me to directly pursue these approaches. The investigation of cardiovascular development is challenging due to its small size, complex geometry, and dynamic physiology. We have taken a variety of approaches to test and define cardiovascular regulatory mechanisms of both normal and defective development, as it is critical to use all available means to solve these formidable obstacles including in silica, in vitro, and in vivo approaches. Using an inducible model of a cardiac defect known as Tetraology of Fallot, we have generated 3D reconstructions of normal and defective hearts throughout development. These models are being used to map the progression of normal and pathological fibrous ECM development. The 3D geometries generated by these studies also serve as inputs for computational simulations that can estimate the mechanical forces present in the developing cardiovascular system and correlate them to ECM expression domains, which are essential for proper cardiac function. Using results from our studies of the molecular mechanisms that regulate ECM deposition discussed below, we are investigating interventions that ameliorate these detrimental affects. These studies are providing much needed avenues for future therapies for cardiovascular birth defects. To directly test the role of hemodynamic forces on developing cardiac valves, we have created an integrated tubular culturing system with a computer-controlled pulsatile fluid flow bioreactor. These studies have found that the localization of several key fibrous ECM proteins, including type I collagen and tenascin-C, is dependent on flow-generated forces and appears to be mediated by the cytoskeletal-associated RhoA pathway. However, other ECM proteins such as periostin appear to be regulated by other small GTPases such as Rac. Thus, to generate valve tissues with the proper functional capabilities, the tissues need to be grown in the correct mechanical environment, which can be accelerated by stimulating the specific small GTPase signaling pathways. Carrying out these studies has provided new insights into the molecular and cellular mechanisms that regulate the generation of the valve ECM architecture that is necessary for proper function. In doing so, we have created a unprecedented model in which to study valve development that has the precision of in vitro studies and the dynamics and three-dimensionality of in vivo tissues. Furthermore, these studies have advanced the ability to generate tissue-engineered valves as requisite ECM deposition has been a limiting factor in current technologies. During the last decade we have created 3D in vitro models of myocardial and coronary vascular development, which have been used to delineate a number of novel molecular mechanisms. Recently, we have created 3D vascular constructs that we are using to gain insight in to the mechanisms that regulate atherogenesis. These studies are in their early stages but have great potential. Another research interest is the use of new materials to drive cellular phenotypes. This interest sprung from our work with biomaterials, such as the collagen tube model, which has been extremely productive. As can be seen from my CV, these research interests have been continuously funded throughout my entire academic career by grants from the National Institutes of Health, National Science Foundation, American Heart Association, and also by industrial sources. Evidence of the innovative nature of our 3D models of cardiovascular development is found in my recent NIH funding. I am confident that we will continue to be the forefront cardiovascular innovation. Lastly, during the first 14 years of my academic career, I have shown that I can develop fruitful collaborations. In the future, I look forward to nourishing existing collaborations and creating new ones at USC Greenville.
Honors & Awards: Paper of the Year
'String of Pearls'Medical Student Teaching Award
'String of Pearls'Medical Student Teaching Award
'String of Pearls'Medical Student Teaching Award
'String of Pearls'Medical Student Teaching Award
Professional Affiliations: Microscopic Society of America
Member
NIH Special Emphasis Panel/Scientific Review Group 2015/01 ZRG1 CVRS-Q (80) A
Member
NIH Special Emphasis Panel/Scientific Review Group 2015/05 ZRG1 BCMB-A (51) R
Member
NIH Special Emphasis Panel/Scientific Review Group 2014/10 ZRG1 CVRS-Q (80) A
Member
NIH Special Emphasis Panel/Scientific Review Group 2013/01 ZRG1 CVRS-K (90)
Member
NIH Special Emphasis Panel/Scientific Review Group 2013/01 ZRG1 CVRS-N (02_ M
Member
NIH Special Emphasis Panel/Scientific Review Group 2013/05 ZRG1 BCMB-A (51) R
Member
NIH NHLBI Ad Hoc Program Project Study Section
Member
American Association of Anatomists
Member
Biomedical Engineering Society
Member
NIH Transformative Research Award program of the NIH Director's Common Fund study section
Member
American Heart Association NAtional Basic Cell and Molecular Biology 2 Study Section
Member
American Heart Association Northeast Affiliate Study Section (ad hoc)
Member