JCB logo
R&D Systems
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
Published online November 19, 2007
doi:10.1083/jcb.200706090
The Journal of Cell Biology, Vol. 179, No. 4, 747-760
The Rockefeller University Press, 0021-9525 $30.00
© 2007 Kümin et al.
This Article
Right arrow Full Text
Right arrow PDF (Full Text)
Right arrow PPT slides of all figures
Right arrow Supplemental Material Index
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kümin, A.
Right arrow Articles by Werner, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kümin, A.
Right arrow Articles by Werner, S.
Related Collections
Right arrowRelated In this Issue article
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Article

 Peroxiredoxin 6 is required for blood vessel integrity in wounded skin

Angelika Kümin1, Matthias Schäfer1, Nikolas Epp1, Philippe Bugnon1, Christiane Born-Berclaz1, Annette Oxenius2, Anke Klippel3, Wilhelm Bloch4, and Sabine Werner1

1 Institute of Cell Biology and 2 Institute of Microbiology, Department of Biology, ETH Zurich, Honggerberg, CH-8093 Zurich, Switzerland
3 Atugen AG, 13125 Berlin, Germany
4 Department of Molecular and Cellular Sport Medicine, German Sport University Cologne, 50927 Cologne, Germany

Correspondence to Sabine Werner: sabine.werner{at}cell.biol.ethz.ch

Peroxiredoxin 6 (Prdx6) is a cytoprotective enzyme with largely unknown in vivo functions. Here, we use Prdx6 knockout mice to determine its role in UV protection and wound healing. UV-mediated keratinocyte apoptosis is enhanced in Prdx6-deficient mice. Upon skin injury, we observe a severe hemorrhage in the granulation tissue of knockout animals, which correlates with the extent of oxidative stress. At the ultrastructural level endothelial cells appear highly damaged, and their rate of apoptosis is enhanced. Knock-down of Prdx6 in cultured endothelial cells also increases their susceptibility to oxidative stress, thus confirming the sensitivity of this cell type to loss of Prdx6. Wound healing studies in bone marrow chimeric mice demonstrate that Prdx6-deficient inflammatory and endothelial cells contribute to the hemorrhage phenotype. These results provide insight into the cross-talk between hematopoietic and resident cells at the wound site and the role of reactive oxygen species in this interplay.

M. Schäfer and N. Epp contributed equally to this paper.

A. Klippel's present address is Wyeth Research, Department of Oncology Discovery, Pearl River, NY 10965.

Abbreviations used in this paper: GO, glucose oxidase; H/E, hematoxylin/ eosin; HUVEC: human umbilical vein endothelial cells; Prdx, peroxiredoxin; ROS, reactive oxygen species; SMA, smooth muscle actin; UV, ultraviolet.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?

Related In this Issue article

Healing skin from within
Mitch Leslie
J. Cell Biol. 2007 179: 568. [Full Text] [PDF]



This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents