Dr Melissa Reichelt

Senior Lecturer

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

Overview

Dr Reichelt is a tenured teaching and research academic in The University of Queensland’s School of Biomedical Sciences. She completed her PhD in cardiovascular Physiology at Griffith University, and held postdoctoral positions at The Victor Chang Cardiac Research Institute (VCCRI) in Sydney, the University of California, San Diego (USA) and was a NHMRC Peter Doherty Postdoctoral Fellow at the University of Melbourne. Dr Reichelt is currently funded by two Australian Research Council Discovery Project Grants and lead a 2019 Major Equipment Infrastructure Grant for a preclinical ultrasound machine (Vevo 3100) which measures cardiac function in animals as small as embryos in utero.

Dr Reichelt investigated the most important receptors governing cardiac function (adenosinergic, adrenergic, angiotensin, growth factor, mineralocorticoid, SGLT2), and the influence of ageing, diabetes, hypertension, exercise, influenza and sepsis on cardiovascular physiology. This work has been published in leading cardiovascular journals including Circulation Research, Basic Research in Cardiology, Cardiovascular Research, Hypertension and broader or other specialist journals such as Autophagy, Antioxidant and Redox Signalling, Journal of Infectious Disease and Scientific Reports. Dr Reichelt’s research has most recently been augmented by in-house design and production of viruses that control the expression of receptors and their ligands. She remains fascinated by what the heart can accomplish; filling with and ejecting blood every second (or so) of every day and night, year after year, while retaining the capacity to more than treble cardiac output during exercise. It’s an incredible feat of engineering and only gets more and more interesting the more I learn about it.

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. This ability to intervene in a time- and cell-subtype-specific manner with gene therapy has many applciations the heart, which are currently being pursued by the Cardiac Disease and Therapy group.

Qualifications

  • Doctor of Philosophy, Griffith University

Publications

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Supervision

  • Doctor Philosophy

  • Doctor Philosophy

  • Doctor Philosophy

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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

Other Outputs

PhD and MPhil Supervision

Current Supervision

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.