Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz

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SHR Neuro Krebs Kardio Stoffw Microb Lipid

TRPC Proteine als Determinanten endothelialer Proliferation

Abstract
Development, maintainance and function of the vascular system requires the ability of endothelial cells to switch between a quiescent, differentiated and a proliferating phenotype, which is able to migrate and form novel capillary tube networks as a key process of angiogenesis. This "angiogenic switch" plays a pivotal role in variety of diseases and is controlled by stimuli that are associated with phospholipase C-mediated Ca2+ entry. Canoncial transient receptor potential (TRPC) proteins are typical downstream targets of phospholipase C signalling providing a route for Ca2+ entry due to formation of homo- and/or heteromeric cation channel complexes.
So far, the role of TRPC channels as determinants of endothelial proliferation, migration and cell-cell adhesion is elusive. The aims in this project are: *To determine which TRPC channel complexes are involved in Ca2+ signalling of proliferation and quiescent endothelial cells, *to characterize the cellular localization and the protein interaction partners of TRPC proteins in these endothelial phenotypes, and to analyze mechanisms of cellular trafficking, assembly and/or disassembly of endothelial TRPC complexes in response to angiogenic stimuli, *to test the concept that specific TRPC signalplexes and processes of cellular TRPC recruitment govern endothelial proliferation, migration and/or integrity of cell-cell junctions.
Lokale Teilprojektleitung:
Sattler Wolfgang
Laufzeit:
01.12.2007-31.07.2010
Programm:
FWF Einzelprojekt
Subprogramm
Hauptprojektleiter an der KFU
Art der Forschung
Grundlagenforschung
Mitarbeiter*innen
Sattler, Wolfgang, Projektleiter*in
Beteiligte MUG-Organisationseinheiten
Lehrstuhl für Molekularbiologie und Biochemie
Gefördert durch
FWF, Fonds zur Förderung der Wissenschaftlichen Forschung, Wien, Österreich

FWF-Grant-DOI: 10.55776/P19820
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