Assistant Staff
Email: [email protected]
Location: Cleveland Clinic Main Campus
My research program is focused on identifying key players in the transition from adaptive to maladaptive remodeling of the heart in response to cardiac injury and metabolic stress. I acquired extensive experience in cell culture, biochemistry, immunofluorescence, microscopy, and electrophysiological techniques while elucidating the molecular mechanisms governing the intra-cellular trafficking and regulation of membrane density of Kv1.5, and how these are altered by pharmaceutical intervention. I have the technical skills for assessing cardiomyocyte function and signaling in vitro, and have focused on elucidating the mechanisms underlying cardiac disease progression and developing therapeutic interventions for human heart failure within the context of in vivo studies. In order to measure and interpret physiological and structural changes in the myocardium, I have developed extensive expertise in cardiac echocardiography, hemodynamic, histologic, and biochemical analysis. I also have experience using primary neonatal and adult cardiomyocytes and genetically modified models to study the molecular mechanisms underlying human cardiovascular disease processes. The overall goal for my research program is to identify novel therapeutic strategies to preserve cardiac structure and function in response to direct cardiac injury and systemic cardiovascular stressors, such as obesity, type II diabetes, and atherosclerosis. One ongoing project is interrogating the underlying disease mechanisms in a novel model of sex-specific heart failure with preserved ejection fraction (HFpEF) and atrial myopathy. In a current R01-supported project, I am interrogating the regulation and relevance of AS160 to cardiomyocyte metabolism, the composition and nature of its protein interactions in healthy versus diseased human and model hearts, and how AS160 signaling in the heart may elicit beneficial effects on systemic metabolic homeostasis. I also serve as Co-Investigator on a P01 project aimed and elucidating mechanistic drivers of atrial fibrillation initiation and progression and using systems and computational biology approaches to identify new therapeutic mechanisms. My lab has extensive experience interrogating cardiac and metabolic stress models and targeting mechanistic drivers to determine therapeutic relevance. My long-term goal and passion is to make significant contributions through teaching, training future scientists, and advancing human therapeutics with an emphasis on cardiovascular signaling and pathogenesis of the heart.
My scientific career began during my undergraduate years at Indiana Wesleyan University (IWU). Through my research under Dr. Burton Webb I gained experience using flow cytometry to detect cell surface markers and quantify differing cell populations from a complex breast cancer tissue sample. This research gave me hands-on experience and an idea of the complexity of pathophysiologic conditions. Dr. Webb was the Associate Dean for the School of Physical and Applied Sciences and Chair of the Division of Natural Sciences and Mathematics. This experience heightened my love of scientific discovery and this passion led me to invest extra hours working as a laboratory technician and under-graduate student instructor all 4 years at IWU. I became determined to pursue a career in science, so in the summer of 2004 I sought an American Society for Pharmacology and Experimental Therapeutics (ASPET) summer fellowship at the University of Michigan in the lab of Dr. Jeffrey Martens, whose excellence in research/teaching led to his recruitment to serve as Chairman of the Department of Pharmacology and Therapeutics at the University of Florida College of Medicine in 2013.
In the spring of 2005 I was accepted to the PhD program in Pharmacology at Michigan. I joined Jeff’s lab because I knew he was an excellent mentor that would challenge me to grow in all areas crucial for a career in research. Jeff was a driven investigator with high standards for the quality and ethical conduct of research, ensuring trainees understood proper controls and how to design the most appropriate experiment for the question being asked. I began my work investigating the mechanisms regulating the intracellular trafficking and membrane expression of the cardiovascular K+ channel Kv1.5. This training enhanced my technical skills in cloning, molecular biology, biochemistry, pharmacology, tissue culture, staining, microscopy, and electrophysiology methods. Moreover, I received invaluable mentoring and experience in writing papers and grants, and delivering effective oral presentations at departmental seminars and national conferences, taking 1st place in the ASPET Cardiovascular Pharmacology Division Junior Scientist Competition. This competition allowed me to pursue membership on the ASPET Cardiovascular Pharmacology executive committee where I assisted in the evaluation and selection of future competitors. This familiarized me with the evaluation processes and highlighted the importance of learning how to identify candidates of outstanding potential. Upon completion of my thesis I was 1st author on a Circulation Research paper and an invited review in Heart Rhythm, 2nd author on a Journal of Biological Chemistry article, and participated in a collaborative project with the laboratory of Dr. Jose Jalife, Co-Director of the Center for Arrhythmia Research at Michigan, that was published in PNAS. In addition, I completed the work for one future 1st author and another middle author Circulation Research paper. During my thesis work I could clearly picture myself as a cardiovascular research scientist in an academic environment. Thus, I decided to pursue a postdoctoral fellowship in a place that would broaden my understanding of cardiac disease and therapeutic research.
This decision led me to the laboratory of Dr. Walter Koch at Temple University School of Medicine. Dr. Koch is a leading researcher in the molecular mechanisms that regulate cardiovascular adrenergic receptor signaling and their role in heart failure, and as Director he provided all of the scientific and professional resources of the Center for Translational Medicine (CTM). Within his lab I have learned echocardiography, trans-aortic constriction (TAC), primary cardiomyocyte isolation, tissue harvesting, histology, RT-qPCR, and to evaluate cardiovascular remodeling and physiology in the context of healthy and diseased animals. I have also written and revised animal protocols and learned how to establish and properly maintain transgenic mouse lines and colonies. In my first project I discovered that the antidepressant drug paroxetine selectively inhibits the G protein-coupled receptor kinase GRK2, reversing cardiac dysfunction in a mouse model of myocardial infarction and producing a 1st author paper in Science Translational Medicine. Thanks to a travel allotment in my Brody Family Medical Trust Fund Fellowship and 2 Temple and 2 conference-sponsored travel awards I have presented my work as a poster or oral competition at 3 national conferences each year. This has allowed me to present my work and begin building a scientific network of experts in cardiovascular research with whom I plan to continue to interact and collaborate as my career progresses. Moreover, I was a finalist in the International Society for Heart Research (ISHR) Young Investigator Award in 2014 and was an invited speaker at the American Heart Association (AHA) Basic Cardiovascular Sciences (BCVS) Meeting in 2014. My current research investigating cardiac-restricted transgenic βARKrgs and βARKnt in a mouse model of pressure overload is expected to result in two additional 1st author publications. The first of these articles, ‘GRK2 RGS Domain-Specific Interaction with Gαq Inhibits Hypertrophy and Cardiac Dysfunction During Pressure Overload’ will be submitted to Science Signaling this fall and has been selected as a finalist for the Melvin L. Marcus Young Investigator Award at AHA Scientific Sessions 2015.
2022 - Present Chair Elect, AHA BCVS Early Career Committee
2021 Benedict R. Lucchesi Young Scientist Travel Award in Cardiac Pharmacology, ASPET, Experimental Biology
2020 - Present Member, International Society for Heart Research (ISHR) North American Section (NAS)
2018 - Present Member, AHA BCVS Early Career Committee
2017 - Present Assistant Professor, Cleveland Clinic Lerner Research Institute, Dept. of Cardiovascular and Metabolic Sciences, Cleveland, OH
2012-2017 Postdoctoral Research Fellow, Temple University, Philadelphia, PA
2017 1st Place, Postdoctoral Scientist Best Abstract Presentation, ASPET Division for Cardiovascular Pharmacology, Experimental Biology
2015 Melvin Marcus Young Investigator Award, AHA Council on Basic Cardiovascular Sciences, AHA Scientific Sessions
2014 Finalist, Young Investigator Awards of the North American Section, International Society for Heart Research (ISHR)
2012 - Present Member, American Heart Association (AHA) Council on Basic Cardiovascular Sciences (BCVS)
2005 - 2011 Graduate Student, University of Michigan, Ann Arbor, MI
2010 1st Place, ASPET Cardiovascular Pharmacology Division Trainee Showcase, ASPET, Experimental Biology
2005 - Present Member, American Society for Pharmacology and Experimental Therapeutics (ASPET)
2001 - 2005 Lab Technician, Undergraduate Student Instructor, & Research Assistant in Biology, Indiana Wesleyan University, Marion, IN
We use a combination of cell culture, pharmacology, proteomics, histology, structure-based drug design, and transgenic models to elucidate the mechanisms that underlie the transition from adaptive to adverse remodeling, including changes in cardiac structure, function, metabolism, fibrosis, and arrhythmogenesis in various models of human disease.
View publications for Sarah Schumacher Bass, PhD
(Disclaimer: This search is powered by PubMed, a service of the U.S. National Library of Medicine. PubMed is a third-party website with no affiliation with Cleveland Clinic.)
1. Manaserh IH, Bledzka KM, Ampong I, Junker A, Grondolsky J, Schumacher SM. A cardiac amino-terminal GRK2 peptide inhibits insulin resistance yet enhances maladaptive cardiovascular and brown adipose tissue remodeling in females during diet-induced obesity. J Mol Cell Cardiol. 2023 Sep 14;183:81-97.
2. Manaserh IH, Bledzka KM, Junker A, Grondolsky J, Schumacher SM. A Cardiac Amino-Terminal GRK2 Peptide Inhibits Maladaptive Adipocyte Hypertrophy and Insulin Resistance During Diet-Induced Obesity. JACC Basic Transl Sci. 2022 Jun;7(6):563-579. PMCID: PMC9270572.
3. Macnee M, Pérez-Palma E, Schumacher-Bass S, Dalton J, Leu C, Blankenberg D, Lal D. SimText: a text mining framework for interactive analysis and visualization of similarities among biomedical entities. Bioinformatics. 2021 Nov 18;37(22):4285-4287. PMCID: PMC9502138.
4. Nagai J, Bellafard A, Qu Z, Yu X, Ollivier M, Gangwani MR, Diaz-Castro B, Coppola G, Schumacher SM, Golshani P, Gradinaru V, Khakh BS. Specific and behaviorally consequential astrocyte G(q) GPCR signaling attenuation in vivo with iβARK. Neuron. 2021 Jul 21;109(14):2256-2274.e9. PMCID: PMC8418870.
5. Bledzka KM, Manaserh IH, Grondolsky J, Pfleger J, Roy R, Gao E, Chuprun JK, Koch WJ, Schumacher SM. A peptide of the amino-terminus of GRK2 induces hypertrophy and yet elicits cardioprotection after pressure overload. J Mol Cell Cardiol. 2021 May;154:137-153. PMCID: PMC8101069.
6. Kwon JS, Schumacher SM, Gao E, Chuprun JK, Ibetti J, Roy R, Khan M, Kishore R, Koch WJ. Characterization of βARKct engineered cellular extracellular vesicles and model specific cardioprotection. Am J Physiol Heart Circ Physiol. 2021 Apr 1;320(4):H1276-H1289. PMCID: PMC8260382.
7. Schumacher SM, Naga Prasad SV. Tumor Necrosis Factor-α in Heart Failure: an Updated Review. Curr Cardiol Rep. 2018 Sep 26;20(11):117. PMCID: PMC6311126.
8. Grisanti LA, Schumacher SM, Tilley DG, Koch WJ. Designer Approaches for G Protein-Coupled Receptor Modulation for Cardiovascular Disease. JACC Basic Transl Sci. 2018 Aug;3(4):550-562. PMCID: PMC6115700.
US Patent | Patent Title | Issue Date | First-Named Inventor |
---|---|---|---|
10835620 | Methods for Treating Heart Failure Using Beta-ARKnt Peptide | 11/17/2020 |
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