AJP - Renal Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Am J Physiol Renal Physiol (February 26, 2002). doi:10.1152/ajprenal.00327.2001
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
283/2/F319    most recent
00327.2001v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ludwig, T.
Right arrow Articles by Schneider, S. W
Right arrow Search for Related Content
PubMed
Right arrow Articles by Ludwig, T.
Right arrow Articles by Schneider, S. W

Articles in PresS, published online ahead of print February 25, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00327.2001
Submitted on October 31, 2001
Accepted on February 19, 2002

Electrical resistance breakdown assay determines role of proteinases in tumor cell invasion

Thomas Ludwig1, Rainer Ossig1, Susanne Graessel2, Marianne Wilhelmi1, Hans Oberleithner1, and Stefan W Schneider1*

1 Department of Physiology, University Muenster, Muenster, NRW, Germany
2 Department of Biochemistry, University Muenster, Muenster, NRW, Germany

* To whom correspondence should be addressed. E-mail: sschnei{at}uni-muenster.de.

The electrical resistance breakdown of the MDCK monolayer provides a continuous assay system for cancer invasion which detects functional changes prior to morphological alterations. Here we address the question whether physical contact between tumor cell and epithelial monolayer is a prerequisite for tumor cell invasion. When human melanoma cells were seeded directly (i.e. physical contact) on top of an electrically tight epithelial cell layer (5800 ± 106 {Omega}cm.2) electrical monolayer leakage led to a 18 ± 3 % reduction of transepithelial electrical resistance within 24h. However, when melanoma cells were seeded close to the basolateral surface of the epithelial cell monolayer but separated by a filter membrane (i.e. no physical contact) electrical leakage occurred even faster (42 ± 3 % reduction in 24 h). Atomic force microscopy detected discrete structural changes between cells. Electrical leakage could be effectively blocked by {alpha}2-macroglobulin or ilomastat, inhibitors of matrix metalloproteinases. We conclude that exocytosis of soluble proteases causes electrical breakdown of the monolayer, independent of physical contact between tumor cells and MDCK monolayer.




This article has been cited by other articles:


Home page
 Cancer Res.Home page
T. Goerge, A. Barg, E.-M. Schnaeker, B. Poppelmann, V. Shpacovitch, A. Rattenholl, C. Maaser, T. A. Luger, M. Steinhoff, and S. W. Schneider
Tumor-derived matrix metalloproteinase-1 targets endothelial proteinase-activated receptor 1 promoting endothelial cell activation.
Cancer Res., August 1, 2006; 66(15): 7766 - 7774.
[Abstract] [Full Text] [PDF]

Home page
 Cancer Res.Home page
E.-M. Schnaeker, R. Ossig, T. Ludwig, R. Dreier, H. Oberleithner, M. Wilhelmi, and S. W. Schneider
Microtubule-Dependent Matrix Metalloproteinase-2/Matrix Metalloproteinase-9 Exocytosis: Prerequisite in Human Melanoma Cell Invasion
Cancer Res., December 15, 2004; 64(24): 8924 - 8931.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 1976 by the American Physiological Society.