Publications by authors named "Wardit Tigchelaar"
Depletion of mitochondrial endo/exonuclease G-like (EXOG) in cultured neonatal cardiomyocytes stimulates mitochondrial oxygen consumption rate (OCR) and induces hypertrophy via reactive oxygen species (ROS). Here, we show that neurohormonal stress triggers cell death in endo/exonuclease G-like-depleted cells, and this is marked by a decrease in mitochondrial reserve capacity. Neurohormonal stimulation with phenylephrine (PE) did not have an additive effect on the hypertrophic response induced by endo/exonuclease G-like depletion.
View Article and Find Full Text PDFArticle Synopsis
- Cardiac hypertrophy leads to changes in heart muscle cells (cardiomyocytes), particularly in their mitochondria, which are crucial for energy production.
- Research showed that stimulation by phenylephrine (PE) reduced mitochondrial efficiency, while insulin-like growth factor 1 (IGF1) improved it, highlighting different effects on heart cell function.
- A gene called Kif5b, which helps position mitochondria, was found to be higher in PE-stimulated cells and in animal models of heart disease, suggesting it plays a key role in how heart cells respond under stress.
Article Synopsis
- The study examined the role of the EXOG gene in cardiac cells, specifically its impact on mitochondrial function and hypertrophy in cardiomyocytes.
- Depleting EXOG in neonatal rat heart cells led to significant hypertrophy without compromising mitochondrial DNA integrity and was linked to increased protein synthesis and elevated mitochondrial respiration rates.
- The findings suggest that loss of EXOG disrupts normal mitochondrial functioning, resulting in heightened mitochondrial respiratory activity and excessive reactive oxygen species (ROS), contributing to cardiomyocyte enlargement.
A kinase interacting protein 1 (AKIP1) is a molecular regulator of protein kinase A and nuclear factor kappa B signalling. Recent evidence suggests AKIP1 is increased in response to cardiac stress, modulates acute ischemic stress response, and is localized to mitochondria in cardiomyocytes. The mitochondrial function of AKIP1 is, however, still elusive.
View Article and Find Full Text PDFCardiac adaptation to unremitting physiological stress typically involves hypertrophic growth of cardiomyocytes, a compensatory response that often fails and causes heart disease. Gene array analysis identified AKIP1 (A Kinase Interacting Protein 1) as a hypertrophic gene and we therefore hypothesized a potential role in the hypertrophic response. We show for the first time that both AKIP1 mRNA and protein levels increased in hypertrophic cardiomyocytes under conditions of sustained cardiac stress, including pressure overload and after myocardial infarction and in vitro in phenylephrine (PE) stimulated neonatal rat ventricular cardiomyocytes (NRVCs).
View Article and Find Full Text PDFAims: Although cardiac diseases account for the highest mortality and morbidity rates in Western society, there is still a considerable gap in our knowledge of genes that contribute to cardiac (dys)function. Here we screened for gene expression profiles correlated to heart failure.
Methods And Results: By expression profiling we identified a novel gene, termed DHRS7c, which was significantly down-regulated by adrenergic stimulation and in heart failure models.