Olga Bondareva (Germany)
Helmholtz Zentrum München
Helmholtz Institute for Metabolic, Obesity and Vascular Research (HI-MAG)
Olga Bondareva completed her Bachelor and Master studies in Applied Mathematics and Physics at the Moscow Institute of Physics and Technology, Russia. She moved to Germany in 2014 to undertake her PhD in Biology as a member of the CiM-IMPRS Joint Graduate Program of the Max Planck Institute for Molecular Biomedicine and the University of Münster. During this time, Olga specialized in vascular biology, epigenetics and bioinformatics. In 2018, she joined the group of Lutz Hein at University of Freiburg for her postdoctoral studies. Here, she further pursued her interests in cardiovascular disease and epigenetics, and established a novel single-cell RNA-sequencing pipeline for the analysis of human cardiomyocytes. In 2020, Olga was recruited to the HI-MAG institute in Leipzig. She has been instrumental in establishing the single cell techniques at the Helmholtz Institute for Metabolism, Obesity and Vascular Research (HI-MAG) and is focused on understanding how metabolic disease causes irreversible damage to blood vessels. Olga Bondareva’s research focuses on vascular dysfunction in diseases associated with metabolic stress and obesity. She is interested in mechanisms of transcriptional regulation and epigenetic control in vascular cells and their implication in the response to various environmental changes. Olga Bondareva’s work is aimed on identification of epigenetic regulators and potential mechanisms of prevention in vascular disease.

Presenter of 1 Presentation

 Conference Calendar

O052 - UNCOVERING IMPACT OF OBESITY ON VASCULATURE IN ORGAN- AND CELL-SUBTYPE SPECIFIC MANNER (ID 151)

Session Name
0760 - Genetic and epigenetic regulatory mechanisms of atherosclerosis (ID 31)
Session Type
Workshop - Pathogenesis of Atherosclerosis
Date
Tue, 23.05.2023
Session Time
15:45 - 17:15
Room
Hall: Heinrich Otto Wieland
Presenter
Lecture Time
16:45 - 16:55

Abstract

Background and Aims

Obesity promotes diverse pathologies, including atherosclerosis and dementia, which frequently involve vascular defects and endothelial cell (EC) dysfunction. Each organ has distinct EC subtypes, but whether ECs are differentially affected by obesity is unknown. Here, we aim to identify organ-specific vulnerabilities of endothelial cells in mouse obesity model.

Methods

We utilize scRNA-seq to analyse transcriptomes of ~375,000 ECs from seven organs in male mice at progressive stages of obesity induced by Western diet. We confirm our findings with orthogonal approaches including immunofluorescent stainings, tracing experiments, and in situ RNA hybridization.

Results

We reveal unique organ- and EC-subtype specific molecular changes driven by obesity, including lipid handling, metabolic pathways, AP1 transcription factor and inflammatory signaling. The transcriptomic aberrations worsen with sustained obesity and are only partially mitigated by dietary intervention and weight loss. By switching obese animals onto a chow diet, we uncover distinct obesity-driven changes in ECs that are responsive or resistant to weight loss. For example, dietary intervention substantially attenuates dysregulation of liver and adipose tissue, but not of kidney EC transcriptomes. Through integration with human GWAS data, we further identify a subset of vascular disease risk genes that are induced by obesity.

Conclusions

Our work catalogues the impact of obesity on the endothelium, and provides a useful resource for further investigation of potential organ-specific vascular therapeutic targets. The data generated in this study are available through an interactive website - https://obesity-ecatlas.helmholtz-muenchen.de.

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