Eintrag vom 19.05.2021
|Für Studierende der:||Medizin, life science|
|voraussichtliche Dauer:||12 Monate|
|ungefährer Arbeitsaufwand:||50-100%, Aug.-Dez. 2021 wird bezahlt|
|Doktorvater / -mutter:||PD Dr. Yuxi Feng|
|Betreuer:||PD Dr. Yuxi Feng/R. Eshwaran|
|Ansprechpartner:||PD Dr. Yuxi Feng|
Beschreibung:Endothelial dysfunction is implicated in the pathogenesis of diabetic complications such as diabetic retinopathy and cardiomyopathy. Our previous data showed that the loss of nucleoside diphosphate kinase (NDPK-B) leads to vascular damage in the mouse retina mimicking diabetic retinopathy. Knockdown of NDPK-B in endothelial cells caused activation of the hexosamine pathway followed by endothelial dysfunction. The data suggest that NDPK-B is an important player contributing to diabetic microvascular dysfunction. Dysregulation of mitochondrial function is directly involved in endothelial dysfunction in the development of diabetic microvascular lesions. However, the mitochondrial function in endothelial cells upon NDPK B modulation and the role of another NDPK isoform – NDPK C are unknown. Thus, the aim of our study is to investigate the mitochondrial function in endothelial cells deficient in NDPK -B and -C.
For this purpose, we will use in vivo and in vitro models, such as NDPK-B or NDPK-C knockout mice, cultured endothelial cells isolated from human umbilical cords. In vitro, candidate genes are knocked down by siRNA.
We are seeking a highly motivated candidate. Our working language is English.