Dr Melissa Reichelt

Lecturer-Physiology

School of Biomedical Sciences
Faculty of Medicine
m.reichelt@uq.edu.au
+61 7 336 52957

Overview

Dr Reichelt undertook her PhD studies in cardiac physiology at the Heart Foundation Research Center at Griffith University, and worked as a postdoctoral research fellow at the Victor Chang Cardiac Research Institute in Sydney. She then worked at The University of California, San Diego before returning to Australia to undertake a National Health and Medical Research Council Peter Doherty Fellowship at the University of Melbourne. Dr Reichelt was then recruited to the University of Queensland working as a postdoctoral fellow for four years, before being appointed as an academic in the School of Biomedical Sciences.

Research Impacts

Dr Reichelt heads the Cardiac Disease and Therapy group, focused on optimising heart function in clinically relevant models of cardiovascular disease including chronic high blood pressure, heart ischemia (lack of flow), diabetes, ageing and cardiotoxicity associated with cancer therapy. Her research spans studies of single cell populations (cell culture), isolated heart function, and function of the intact heart. This approach is integrated with advanced techniques for gene editing to target specific cell subtypes in the heart to modify receptor expression and function.

Qualifications

  • Doctor of Philosophy, Griffith University

Publications

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Available Projects

  • Cardiac enlargement is essential for normal maturation, and adaptation to exercise. It also occurs in pathological settings such as chronic hypertension. We are interested in the role that two receptors play in this response; ErbB1 also known as the Epidermal Growth Factor Receptor (EGFR) and it’s sibling ErbB4. We use adeno-associated viruses (AAV) in animals with floxed animals to delete our receptors of interest in a time and cell subtype specific manner and examine the impact on heart enlargement.

    Multiple research projects are available for this large project which would involve some small animal work, immunohistochemistry, qPCR, western blot, isolated heart experiments (langendorff), cell culture and in vivo assessment of heat function (echocardiography) depending on student preferences.

  • The ability of the ventricle relax and expand to fill with blood in diastole is essential to normal heart function. Diastolic dysfunction, where cardiac filling is impaired, occurs in a number of clinical pathologies including heart failure with preserved ejection fraction (HFpEF) and diabetes. We recently published the first evidence that a membrane protein essential to sensing stretch, called cavin is essential to normal diastolic tone. Hearts from Cavin knockout animals are stiff and unable to detect stretch, and we were able to demonstrate that this was due to elevation of nitric oxide. We are now looking to translate this finding in animals into human heart tissues, through a collaboration with the Prince Charles Hospital. We are also intested in seeing if stiffness is also present mice lacking another membrane protein, Caveolin, and what heart cell-subtypes are the most important.

    This project could involve work at Prince Chales Hospital on fresh human heart tissue (tranbeculae that are removed as a part of some surgical procedures), or could involve isolated heart experiments in Caveolin 1 and 3 knockout mice. Both projects would also involve real time PCR of RNA isolated from tissues, western blot, immunohistochemistry and nitric oxide and nitrosylation assays.

View all Available Projects

Publications

Featured Publications

Journal Article

Conference Publication

Possible Research Projects

Note for students: The possible research projects listed on this page may not be comprehensive or up to date. Always feel free to contact the staff for more information, and also with your own research ideas.

  • Cardiac enlargement is essential for normal maturation, and adaptation to exercise. It also occurs in pathological settings such as chronic hypertension. We are interested in the role that two receptors play in this response; ErbB1 also known as the Epidermal Growth Factor Receptor (EGFR) and it’s sibling ErbB4. We use adeno-associated viruses (AAV) in animals with floxed animals to delete our receptors of interest in a time and cell subtype specific manner and examine the impact on heart enlargement.

    Multiple research projects are available for this large project which would involve some small animal work, immunohistochemistry, qPCR, western blot, isolated heart experiments (langendorff), cell culture and in vivo assessment of heat function (echocardiography) depending on student preferences.

  • The ability of the ventricle relax and expand to fill with blood in diastole is essential to normal heart function. Diastolic dysfunction, where cardiac filling is impaired, occurs in a number of clinical pathologies including heart failure with preserved ejection fraction (HFpEF) and diabetes. We recently published the first evidence that a membrane protein essential to sensing stretch, called cavin is essential to normal diastolic tone. Hearts from Cavin knockout animals are stiff and unable to detect stretch, and we were able to demonstrate that this was due to elevation of nitric oxide. We are now looking to translate this finding in animals into human heart tissues, through a collaboration with the Prince Charles Hospital. We are also intested in seeing if stiffness is also present mice lacking another membrane protein, Caveolin, and what heart cell-subtypes are the most important.

    This project could involve work at Prince Chales Hospital on fresh human heart tissue (tranbeculae that are removed as a part of some surgical procedures), or could involve isolated heart experiments in Caveolin 1 and 3 knockout mice. Both projects would also involve real time PCR of RNA isolated from tissues, western blot, immunohistochemistry and nitric oxide and nitrosylation assays.