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Protein Expression of ATP Synthase Regulators in Pressureoverload Induced Cardiac Hypertrophy

Undergraduate #51
Discipline: Biological Sciences
Subcategory: Cell and Molecular Biology

Terry McCollough - Lawson State Community College/ University of Alabama at Birmingham
Co-Author(s): Yishu Ding and Qinglin Yang, University of Alabama at Birmingham, Birmingham, AL



Energy metabolism plays an essential role in the energydemanding heart. ATP synthase is a key molecular motor that plays a key role in determining the energy state of cells. This is particularly important for proper functioning of the heart. Therefore, optimizing cardiac energy metabolism has long been a major therapeutic target for treating cardiac pathologies. The ATP synthase activity can be regulated by endogenous regulation of proteins. A natural ATP synthase inhibitor, IF1, is known to block the ATP hydrolysis direction of the ATP synthase to promote ATP reservation. Our lab has recently discovered a novel protein ES1 that can modulate ATP synthase activity and plays a protective role in the hypertrophied heart. As far as methods, three month old male mice (C57/B6) mice were allocated to two experimental groups. Protein extraction and SDS-PAGE gel Electrophoresis and a western blot analysis were the other methods used in the study. In conclusion, the protein expression of the two important regulators of ATP synthase, IF1 and ES1, in the hypertrophied hearts induced by TAC-induced pressure overload does change. Given the potential importance of IF1 and ES1 in determining myocardial energy metabolism, the objective of my research project is to investigate the protein expression of IF1 and ES1 in the hypertrophied heart as induced by transverse aortic constriction (TAC)-induced pressure overload. Future directions for this ongoing project is to assess the cardiac expression of IF1 and ES1 on mice with longer term of TAC-induced cardiac hypertrophy to see if these proteins play a role in determining myocardial energy at later stage of the pathological development.

Funder Acknowledgement(s): NSF

Faculty Advisor: Qinglin Yang,

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This material is based upon work supported by the National Science Foundation (NSF) under Grant No. DUE-1930047. Any opinions, findings, interpretations, conclusions or recommendations expressed in this material are those of its authors and do not represent the views of the AAAS Board of Directors, the Council of AAAS, AAAS’ membership or the National Science Foundation.

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