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Headshot photo of Fikru Belema Bedada

Fikru Belema Bedada

Associate Professor

  • Clinical Laboratory Science
  • College of Nursing and Allied Health Sciences


Dr Fikru B. Bedada is an assistant professor at the department of clinical laboratory sciences (CLS), college of nursing and allied health sciences, Howard university. His primary responsibilities include teaching didactic and laboratory aspects of core disciplines offered at the CLS department such as

  1. Clinical Biochemistry and Instrumentation CLLS 309,
  2. Clinical Chemistry II CLLS 410
  3. Clinical Chemistry Practicum CLLS 408 and 
  4. Molecular Diagnostics CLLS 400

In this endeavor, he advises and mentors his students to foster retention, progression and professional competencies. Dr Bedada is certified MLS (ASCPi) by the American Society for Clinical Pathology (ASCP) Board of Certification (BOC).

Dr Bedada research intersect is centered on basic research and translational research.

In his strive towards basic research, Dr Bedada has extensive collaborative interdisciplinary research experience in the areas of embryonic stem cells (ESCs), human induced pluripotent stem cells (hiPSCs), adult stem cells and their differentiation into mesoderm such as striated and cardiac muscle cells. He has acquired and developed such skills and knowledge through graduate and postdoctoral research training under the mentorship of Dr. Thomas Braun, Max Planck Institute and with Dr. Joseph Metzger, university of Minnesota. Dr Bedada has worked on normal and patient-derived human iPSCs which can be modeled as “Patient in Dish” and play critical role in personalized medicine. Dr Bedada has worked in a project that addresses an increasingly apparent disconnect in understanding the concept of cardiac maturation in human. He advanced the field by investigating the molecular signature defining cardiac myocyte maturation.

Dr Bedada has also gained experience in therapeutic gene delivery using adenoviral and recombinant adeno associated virus (rAAV) gene delivery systems into the adult heart. He has over 15 years of molecular and cellular biology experience. Dr. Bedada has collaborated with leading experts in the NIH directed Progenitor Cell Biology Consortium (PCBC). He has published a total of 15 high profile papers, notably a high impact paper published in Cell Stem Cell.

Dr. Bedada has made several exciting progresses in the field of cardiovascular system by investigating the maturation process of human cardiac myocytes that is vital for in vitro drug testing, disease modeling, future cell-based therapy and personalized medicine. He has embarked in the state-of-the-art genetic engineering techniques such as Transcription activator-like (TAL) effectors nuclease (TALEN), Zink finger nuclease (ZFN) and Clustered regularly interspaced short palindromic repeats (CRISPR-Cas9) and CRISPR-dCas9 interference technologies. He has additional experience with genome editing in human induced pluripotent stem cells using new tools including TALEN, ZFN, and CRISPR/Cas9 based genome editing.  He has engineered multiple novel human iPSC cell lines, including novel drug-titratable gene expression systems.

In his endeavor towards translational research, Dr Bedada’s overall goal is to provide evidence that can be used to predict disease progression and response to exercise intervention in elderly AAs with MCI.

In this regard, Dr Bedada’s research interest is also focused on identifying and characterizing biomarkers of myopathy, cardiomyopathy, cellular clearance, inflammation and their link with aging and age-related diseases such as neurodegeneration and how exercise intervention impacts gene expression profile to provide beneficial outcome in elderly African Americans (AA)s with Mild Cognitive Impairment (MCI). He is particularly interested in component of ubiquitin proteasome system (UPS) such as FBXO32, TRIM63, and transcription factors, FOXOs.

Dr Bedada is also investigating the H2S, SIRT1 and Insulin/IGF-1 signaling (IIS) pathways. He tests the hypothesis that exercise induced expression of homocysteine metabolizing enzymes such as cystathionine-β-synthase (CBS) and cystathionine-γ-lyase (CTH) which are linked to delay pace of cellular senescence can be beneficial during aging and neurodegeneration. CBS and CTH are precursor enzymes for the biosynthesis of H2S, a potent cellular protector. Dr Bedada’s goal is to provide evidence that exercise induced CBS, CTH and splice factors expression can be beneficial and enhance declining metabolic competencies manifested during aging and age-related diseases by way of H2S, SIRT1 and Insulin/IGF-1 signaling (IIS) pathways.

Education & Expertise


Cellular and Molecular Biology

Martin Luther University at Halle (Saale), Germany

Molecular Biology

Free University of Brussels (VUB), Belgium

Medical Laboratory Technology

Jimma Institute of Health Sciences (JIHS), Ethiopia

Related Articles

Peer-reviewed Publications:

1.       Wheelwright M, Mikkila J, Bedada FB, Mandegar MA, Thompson BR, Metzger JM. Advancing physiological maturation in human induced pluripotent stem cell-derived cardiac muscle by gene editing an inducible adult troponin isoform switch. Stem Cells 2020 Jun 04;10.1002/stem.3235.2.       Bedada FB, Martindale JJ, Arden E, Metzger JM. Molecular inotropy mediated by cardiac miR-based PDE4D/PRKAR1alpha/phosphoprotein signaling. Sci Rep 2016;6:36803.3.       Martire A, Bedada FB, Uchida S, et al. Mesenchymal stem cells attenuate inflammatory processes in the heart and lung via inhibition of TNF signaling. Basic Res Cardiol 2016;111:54.4.       Bedada FB, Wheelwright M, Metzger JM. Maturation status of sarcomere structure and function in human iPSC-derived cardiac myocytes. Biochim Biophys Acta 2015;1863:1829-38.5.       Barnabei MS, Sjaastad FV, Townsend D, Bedada FB, Metzger JM. Severe dystrophic cardiomyopathy caused by the enteroviral protease 2A-mediated C-terminal dystrophin cleavage fragment. Sci Transl Med 2015;7:294ra106.6.       Bedada FB, Chan SS, Metzger SK, et al. Acquisition of a quantitative, stoichiometrically conserved ratiometric marker of maturation status in stem cell-derived cardiac myocytes. Stem Cell Reports 2014;3:594-605.7.       Rasmussen TL, Kweon J, Diekmann MA, Bedada FB, et al. ER71 directs mesodermal fate decisions during embryogenesis. Development 2011;138:4801-12.8.       Palpant NJ, Bedada FB, Peacock B, Blazar BR, Metzger JM, Tolar J. Cardiac disease in mucopolysaccharidosis type I attributed to catecholaminergic and hemodynamic deficiencies. Am J Physiol Heart Circ Physiol 2010;300:H356-65.9.       Palpant NJ, Szatkowski ML, Wang W, Bedada FB, et al. Artificial selection for whole animal low intrinsic aerobic capacity co-segregates with hypoxia-induced cardiac pump failure. PLoS One 2009;4:e6117.10.     Turner I, Belema-Bedada F, Martindale J, et al. Molecular cardiology in translation: gene, cell and chemical-based experimental therapeutics for the failing heart. J Cardiovasc Transl Res 2008;1:317-27.11.     Belema-Bedada F, Uchida S, Martire A, Kostin S, Braun T. Efficient homing of multipotent adult mesenchymal stem cells depends on FROUNT-mediated clustering of CCR2. Cell Stem Cell 2008;2:566-75.12.     Bedada FB, Braun T. Partial induction of the myogenic program in noncommitted adult stem cells. Cells Tissues Organs 2008;188:189-201.13.     Bedada FB, Gunther S, Kubin T, Braun T. Differentiation versus plasticity: fixing the fate of undetermined adult stem cells. Cell Cycle 2006;5:223-6.14.     Belema Bedada F, Technau A, Ebelt H, Schulze M, Braun T. Activation of myogenic differentiation pathways in adult bone marrow-derived stem cells. Mol Cell Biol 2005;25:9509-19.15.     Schulze M, Belema-Bedada F, Technau A, Braun T. Mesenchymal stem cells are recruited to striated muscle by NFAT/IL-4-mediated cell fusion. Genes Dev 2005;19:1787-98.