Nauta 2016 Thesis

From Bioblast
Publications in the MiPMap
Nauta TD (2016) HIF-2Ξ± regulates in vitro neovascularization during hypoxia. Doctoral Dissertation p206.

Β» Open Access

Nauta TD (2016) Doctoral Dissertation

Abstract: Blood vessels are crucial in the mammalian body for the delivery of oxygen, nutrients and signaling molecules, such as hormones, to cells and the removal of waste product from these cells. Endothelial cells (ECs) line the entire vasculature. In the healthy body, most ECs are quiescent; the cells hardly divide. Nonetheless, the endothelium performs many physiological functions, such as vasoregulation by producing vasoactive factors including nitric oxide (NO) and endothelin-1 (ET-1) required for adequate distribution of blood between the tissues; formation of a barrier between blood and surrounding tissues that allows optimal exchange of oxygen, nutrients and hormones; hemostasis; and the recruitment of leukocytes at sites of inflammation (3). Dysfunction of the endothelium is associated with many diseases, such as atherosclerosis, hypertension, thrombosis and improper inflammatory activation of tissues; endothelial barrier dysfunction leads to vascular leakage, which is related to pathological conditions, including sepsis (21), acute lung injury (47), and cancer (25). Improper functioning of tissues often results in inadequate perfusion and the need for additional blood supply. This can occur by neovascularization, a process in which endothelial cells play a central role. This thesis investigates the effect of long-term hypoxia on the response of endothelial cells that leads to improved vascularization.

β€’ Bioblast editor: Kandolf G β€’ O2k-Network Lab: NL Amsterdam Wuest RC


Labels: MiParea: Respiration 

Stress:Oxidative stress;RONS, Hypoxia  Organism: Human  Tissue;cell: Endothelial;epithelial;mesothelial cell  Preparation: Intact cells 


Coupling state: LEAK, ROUTINE, ET  Pathway: ROX  HRR: Oxygraph-2k 


Cookies help us deliver our services. By using our services, you agree to our use of cookies.