Prof. Dr. Dietmar Vestweber

Molecular mechanisms that control endothelial junctions and leukocyte extravasation

Blood vessel in the cremaster tissue stained for an endothelial antigen (green) and a leukocyte antigen (red).
© Vestweber

Cell Biology / Molecular Biology
Immunology
Vascular Biology / Angiogenesis   


Leukocyte entry into tissue is usually triggered by pathological stimuli such as physical injury or infectious microorganisms. It is the starting event that initiates the process of inflammation and that controls the continuation of inflammatory reactions. Understanding its molecular basis will allow to interfere with and modulate the often harmful consequences of the inflammatory process. Within this context we are investigating the molecular mechanism that enables leukocytes to overcome the blood vessel wall mainly formed by endothelial cells, a basement membrane and associated perivascular cells. We are presently focusing on novel endothelial membrane proteins that control the endothelial barrier function during leukocyte extravasation.

Possible projects for a PhD thesis:
- Endothelial signaling mechanisms that counteract inflammation by stabilizing endothelial cell junctions
- Diversity of endothelial junctions in the vasculature of different tissues
- The role of VE-cadherin and associated binding partners for vascular integrity
- Leukocyte diapedesis: how leukocytes adhere to and crawl through the endothelial barrier

 

 

Prof. Dr. Dietmar Vestweber
Prof. Dr. Dietmar Vestweber
Max Planck Institute for Molecular Biomedicine
Röntgenstraße 20
48149 Münster
T: +49 (0) 251- 70365 210
F: +49 (0) 251- 70365 299
vestweb@mpi-muenster.mpg.de

Vita

  • 1976 - 1982: Studies in Biochemistry, Eberhard-Karls-Universität, Tübingen
  • 1983 - 1985: Dissertation at the Friedrich Miescher-Laboratory of the Max-Planck-Society
  • 1987 - 1989: "Postdoctoral Fellow" at the Biocenter, University of Basel, Switzerland
  • 1990 - 1994: Head of an independent research group at the Hans-Spemann-Laboratory of the Max-Planck-Institute for Immunobiology in Freiburg
  • 1994 - 2006: Full Professor for Cell Biology (C4) at the University of Münster
  • 1998: Gottfried Wilhelm Leibniz Award of the DFG
  • 1999 - 2001: Director at the Max-Planck-Institute  for physiological und clinical Research , Bad Nauheim
  • Since 2001: Founding-Director of the “Max-Planck-Institute for Vascular Biology”, renamed in 2004 as “MPI for Molecular Biomedicine”, Münster
  • 2002: Elected Member of the German Academy of Science, Leopoldina
  • 2009: Elected member of EMBO

Selected references

Arif N, Zinnhardt M, Nyamay’Antu A, Teber D, Brückner R, Schäfer K, Li Y-T, Trappmann B, Grashoff C, Vestweber D. (2021) PECAM-1 supports diapedesis by tension-dependent dephosphorylation of VE-cadherin. EMBO J. in press

Braun LJ, Stegmeyer R, Schäfer K, Volkery S, Currie SM, Kempe B, Nottebaum AF,
Vestweber D. (2020) Platelets docking to VWF prevent leaks during leukocyte extravasation by stimulating Tie-2. Blood, 136(5): 627-639

Frye M, Dierkes M, Küppers V, Vockel M, Tomm J, Zeuschner D, Rossaint J, Zarbock A, Koh GY, Peters K, Nottebaum AF, Vestweber D. (2015) Interfering with VE-PTP stabilizes endothelial junctions in vivo via Tie-2 in the absence of VE-cadherin. J Exp Med 212(13): 2267-2287

Vestweber D. (2015) How leukocytes cross the vascular endothelium.  Nat Rev Immunol 15:692-7014

Wessel F, Winderlich M, Holm M, Frye M, Rivera-Galdos R, Vockel M, Linnepe R, Ipe U, Stadtmann A, Zarbock A, Nottebaum A, Vestweber D (2014). Leukocyte extravasation and vascular permeability are each controlled in vivo by a different tyrosine residue of VE-cadherin. Nat Immunol 15(3): 223-230

Links

Vestweber Lab