Publikationsdatenbank

VIM, TPI, MAT2A and their role in in vitro angiogenesis (2023)

Art

Vortrag

Autoren

Herre, C. (WE 1)

Nshdejan, A. (WE 1)

Klopfleisch, R. (WE 12)

Corte, G. M.

Bahramsoltani, M. (WE 1)

Kongress

XXXIV EAVA Congress 2023

Sundvollen, Norway, 25. – 29.07.2023

Quelle

The XXXIV EAVA-congress at Sundvolden hotel 2023 : congress program & book of abstracts — NMBU Norwegian University of Life Sciences, EAVA (Hrsg.)

— S. 23

Sprache

Englisch

Verweise

URL (Volltext): https://main-bvxea6i-kdsvgmpf4iwws.eu-5.platformsh.site/sites/default/files/2023-07/Book%20of%20abstracts_4.pdf

Kontakt

Institut für Tierpathologie

Robert-von-Ostertag-Str. 15
14163 Berlin
+49 30 838 62450
pathologie@vetmed.fu-berlin.de

Abstract / Zusammenfassung

As a requirement for versatile pathological events, e.g. tumorigenesis, endothelial cells (ECs) are compelled to perform angiogenesis. The research field of angiogenesis is currently focusing on tissue engineering and wound healing. Putatively based on the heterogenous character of ECs, in vitro assays of angiogenesis still face difficulties considering their reproducibility. Morphologically classified into angiogenic and non-angiogenic, ECs revealed alterations in their expression of eight specific proteins (1). Among them, vimentin (VIM), triosephosphate isomerase (TPI) and adenosylmethionine synthetase isoform type-2 (MAT2A), are selected for this study in order to get analyzed considering their association to in vitro angiogenesis. Therefore, tip and stalk cell distribution within cell populations of human dermal microvascular endothelial cells were analyzed via VEGFR-1 and -2 expression. A shRNA mediated knockdown of VIM and TPI was initiated separately. Cells were long-term cultivated using proangiogenic media and morphologically staged
into their respective angiogenic stage, according to the all-in-one assay (2). During cultivation, protein and mRNA expression profiles of VIM, TPI and MAT2A were determined. Native cells displayed a high expression of VIM and MAT2A in early angiogenic stages and TPI throughout angiogenesis in
vitro. VIM and TPI knockdown, respectively, resulted in cells not being able to enter late stages of in vitro angiogenesis, opposed to native ECs. By knocking down VIM, only cells with higher VEGFR-1 expression survived showing an increase in MAT2A and TPI expression. Concluding that VIM and
MAT2A are indicated to be relevant in beginning stages and TPI during the course of angiogenesis in vitro. VIM and TPI knockdown led to a deceleration of in vitro angiogenesis, whereby knocking down VIM resulted in cell death of populations with less stalk cells and alterations of TPI and MAT2A expression.