Neuronostatin, connective tissue growth factor and glycogen synthase kinase 3β in cardiac physiology and disease.

Thesis event information

Date and time of the thesis defence

Place of the thesis defence

Auditorium F202 of the Faculty of Medicine (Aapistie 5 B). Remote access: https://oulu.zoom.us/j/69875616000?pwd=TDdTbzE3Z1VSbzVXSmN6RVpNa3R2UT09

Topic of the dissertation

Neuronostatin, connective tissue growth factor and glycogen synthase kinase 3β in cardiac physiology and disease.

Doctoral candidate

Licentiate of Medicine Laura Vainio

Faculty and unit

University of Oulu Graduate School, Faculty of Medicine, Biomedicine

Subject of study

Pharmacology

Opponent

Professor Anna-Liisa Levonen, University of Eastern Finland

Custos

Professor Risto Kerkelä, University of Oulu

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Neuronostatin, connective tissue growth factor and glycogen synthase kinase 3β in cardiac physiology and disease.

Cardiovascular diseases are the leading cause of death in Western countries and new, more targeted therapeutical approaches are needed. The aim of my thesis was to increase understanding of the signaling pathways regulating progression of cardiac remodeling from myocardial infarction injury and cardiac hypertrophy to heart failure. In these preclinical studies, I focused on the factors regulating cardiomyocyte survival, hypertrophy and extracellular matrix modulation; neuronostatin (NST), connective tissue growth factor (CTGF), and glycogen synthase kinase 3β (GSK3β). I found that NST has an attenuating effect on left ventricular contractility in isolated perfused rat heart and it also reduced survival of the cultured cardiomyocytes. Therapy with a CTGF monoclonal antibody improved recovery after myocardial infarction in mice. Phosphorylation of the GSK3β S389 site was cardioprotective and antihypertrophic in cultured cardiomyocytes. I also dissected the cellular signaling mechanisms regulated by these factors. This study reveals novel biological functions and signaling mechanisms for these factors and may eventually lead to development of targeted therapies to decrease and prevent cardiac injury.
Last updated: 28.5.2021