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"Faces" of the day:

Katharina Jandl

Nina Höller

Nariae Baik-Schneditz

Ellen Heitzer

Marianne Brodmann

Ewald Kolesnik

Bernhard Schwaberger

Maximilian Seles

Gabor Toth-Gayor

Lukas Peter Mileder

Niels Hammer

Christian Josef Hill

Christian Viertler

Philipp Klaritsch

Daniel Scherr

Harald Köfeler

Gerhard Pichler

Roland Malli

Michael Fuchsjäger

Gernot Plank

Peter Fickert

Richard Zigeuner

Peter Holzer

Selected Publication:

SHR Neuro Cancer Cardio Lipid Metab Microb

Strahlhofer-Augsten, M; Schliefsteiner, C; Cvitic, S; George, M; Lang-Olip, I; Hirschmugl, B; Marsche, G; Lang, U; Novakovic, B; Saffery, R; Desoye, G; Wadsack, C.
The Distinct Role of the HDL Receptor SR-BI in Cholesterol Homeostasis of Human Placental Arterial and Venous Endothelial Cells.
Int J Mol Sci. 2022; 23(10): 5364 Doi: 10.3390/ijms23105364 [OPEN ACCESS]
Web of Science PubMed FullText FullText_MUG

 

Leading authors Med Uni Graz

Schliefsteiner Carolin

Strahlhofer-Augsten Manuela Herta

Wadsack Christian

Co-authors Med Uni Graz

Desoye Gernot

George Meekha

Hirschmugl Birgit

Lang Uwe

Lang-Olip Ingrid

Marsche Gunther

Tokic Silvija

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Abstract:

As opposed to adults, high-density lipoprotein (HDL) is the main cholesterol carrying lipoprotein in fetal circulation. The major HDL receptor, scavenger receptor class B type I (SR-BI), contributes to local cholesterol homeostasis. Arterial endothelial cells (ECA) from human placenta are enriched with cholesterol compared to venous endothelial cells (ECV). Moreover, umbilical venous and arterial plasma cholesterol levels differ markedly. We tested the hypothesis that the uptake of HDL-cholesteryl esters differs between ECA and ECV because of the differential expression of SR-BI. We aimed to identify the key regulators underlying these differences and the functional consequences. Immunohistochemistry was used for visualization of SR-BI in situ. ECA and ECV were isolated from the chorionic plate of human placenta and used for RT-qPCR, Western Blot, and HDL uptake assays with ³H- and ¹²⁵I-labeled HDL. DNA was extracted for the methylation profiling of the SR-BI promoter. SR-BI regulation was studied by exposing ECA and ECV to differential oxygen concentrations or shear stress. Our results show elevated SR-BI expression and protein abundance in ECA compared to ECV in situ and in vitro. Immunohistochemistry demonstrated that SR-BI is mainly expressed on the apical side of placental endothelial cells in situ, allowing interaction with mature HDL circulating in the fetal blood. This was functionally linked to a higher increase of selective cholesterol ester uptake from fetal HDL in ECA than in ECV, and resulted in increased cholesterol availability in ECA. SR-BI expression on ECV tended to decrease with shear stress, which, together with heterogeneous immunostaining, suggests that SR-BI expression is locally regulated in the placental vasculature. In addition, hypomethylation of several CpG sites within the SR-BI promoter region might contribute to differential expression of SR-BI between chorionic arteries and veins. Therefore, SR-BI contributes to a local cholesterol homeostasis in ECA and ECV of the human feto-placental vasculature.

Find related publications in this database (Keywords)

human placenta

SR-BI

HDL

endothelium

arterial-venous difference

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