Wound Healing MDC Researchers Identify Key Function of a Molecule
When the
skin is injured, it first scabs over as a first aid measure, so-to-speak,
sealing the wound to keep germs out. Starting from the edge of the wound,
keratinocytes then migrate across the wound. They proliferate especially
quickly, thereby rapidly forming new skin tissue which covers the wound in a
short time. This very fast growing tissue, the hyperproliferative epithelium,
also fills up the wound with new skin cells so that finally new tissue is
formed which replaces the scab.
The signal
molecule, c-Met, regulates this migration process from the edge of the wound.
It is a receptor molecule also localized on epithelial cell membranes. The role
c-Met plays in developmental biology has been studied intensively during the
past years by Professor Carmen Birchmeier and her research team. Interacting with
c-Met is a growth factor given the name hepatocyte growth factor/scatter factor
(HGF/SF) because it was discovered to be a growth factor in liver cells
(hepatocytes). The liver is an organ that regenerates especially quickly after
injury. In cancer research, this factor also plays a key role as scatter
factor, which Professor Walter Birchmeier and his colleagues were repeatedly
able to demonstrate.
The duo
HGF/SF and c-Met is crucial in regulating cell migration. Together, the two are
not only released in the liver, but also in the lung, the kidneys, and the
heart when these organs are injured. As MDC researchers were now able to show,
this is also the case with skin wounds: HGF/SF and c-Met are increasingly
released by the hyperproliferative skin tissue. Hence, this tissue promotes its
own growth. However, while c-Met is normally found in both the skin and the
hair follicles (and in wounds is
increasingly released in the hyperproliferative epithelium), HGF/SF is proven
to be present prior to injury in the hair follicles but not in the skin. HGF/SF
is not active in the skin until after an injury at which time it is
particularly active at the wound edges of the hyperproliferative epithelium.
With a
special technique, the MDC researchers specifically deactivated the gene for
c-Met in mice. They discovered that mice whose skin cells no longer produce
c-Met do not form new skin when the skin is injured. In mice that still have
some skin cells with active c-Met, because these cells escaped the genetic mutation,
wound healing is not blocked. However, it starts later and takes twice as long
as in the normal case. That means that only skin cells with active c-Met can
build up fast-growing, protective new tissue to close a skin wound.
*c-Met is essential for wound
healing in the skin
Jolanta Chmielowiec1,
Malgorzata Borowiak2, Markus Morkel1, 6, Theresia Stradal3,
Barbara Munz4, Sabine Werner5, Jürgen Wehland3,
Carmen Birchmeier2, Walter Birchmeier1*
1Department of Cancer Biology, Max
DelbrückCenter
for Molecular Medicine, Robert-Rössle-Strasse 10, 13125 Berlin, Germany
2Department of Neuroscience, Max
DelbrückCenter
for Molecular Medicine, Robert-Rössle-Strasse 10, 13125 Berlin, Germany
3Department of Cell Biology, Helmholtz Centre for Infection Research, Mascheroder
Weg 1, 38124 Braunschweig, Germany
4Institute of Physiology, Charité‑Medical University Berlin, Arnimallee 22, 14195 Berlin, Germany
5Institute of Cell Biology, ETH Zurich,
Hönggerberg, CH-8093 Zurich,
Switzerland
6Present address: Max Planck Institute for Molecular Genetics,
Ihnestrasse 73, 14195 Berlin, Germany
*Corresponding author: Walter Birchmeier
Phone: +49-30-94063810, Fax: +49-30-94062656; E-mail:
Barbara Bachtler
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