Vortrag von Mara Pitulescu
Vortragstitel: "Role of cell-cell communication in organ-specific vasculature"
Anlass: SFB Seminar
Host: Kerstin Bartscherer
Beginn: 06.07.2023 - 16:15 Uhr
Ort: CellNanOs, 38/201
Über die Vortragende: Mara Pitulescu forscht am Max Planck Institut für molekulare Biomedizin in Münster.
Inhalt des Vortrags: The vasculature is a hierarchical network composed of arteries, veins and capillaries, which plays a critical role in maintaining the health and ensuring the metabolic demands and functionality of every organ in the human body. Endothelial cells, lining the inner surface of vessels, exhibit remarkable heterogeneity and functional specialization across different organs.
Thus, in heart, a highly vascularized organ, capillary endothelial cells through their direct communication with cardiomyocytes, ensure sufficient supply of nutrients and oxygen. Eph receptors and their ephrin ligands are essential regulators of cell-cell interactions, mediating repulsion, adhesion and migration processes. Using mouse genetics, imaging and cell biology approaches we addressed how homeostasis in the adult heart is controlled by endothelial EphB4/ephrin-B2 signaling. Among cardiovascular diseases, arterial-derived pathology leads to much severe disease progression such as stroke, coronary artery disease or pulmonary arterial hypertension. However, while the importance of artery formation and function is widely appreciated, the underlying cellular and molecular mechanisms remain little understood for most organs.
Our recent work in murine retina uncovered a novel mechanism of artery extension, in which progeny of ESM1+ endothelial tip cells, which lead vessel sprouts in the growing vasculature, is directed into arteries and mediates artery expansion. In vascular endothelium, ephrin-B2 marks arteries, while EphB4 predominantly labels veins. While both molecules are expressed by endothelial sprouts, we explored the possibility that their interactions control cell sorting processes contributing to the specification of future arterial ECs. Furthermore, ESM1+ progenitor cells are induced in specific microenvironments, or niches, at considerable distance from existing arteries. Thus, using genetically modified mice, confocal microscopy and next generation sequencing, we also investigated if this involves both common but also organ-specific mechanisms.