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Department
of Gastroenterology, Juntendo University School of Medicine, Tokyo,
Japan
Correspondence to: Professor N Sato, Department of Gastroenterology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan.
Accepted for publication 18 March 1999
BACKGROUND
Various
factors affect gastric wound healing. The influence of physical
stimulation on gastric mucosal cells during the process of gastric
wound healing is not completely understood.
AIMSTo assess the
role of a physical stimulant, in this case mechanical strain, on
gastric mucosal restoration.
METHODSMechanical
strain was applied to adherent rat gastric mucosal cells (RGM1)
cultured confluently on collagen type I coated silicone elastomer
membrane in order to increase the dimension by an average of 5% and
10% at 5 cycles/minute for 72 hours after wounding. Repair of the
wound was monitored every 12 hours for up to 72 hours using an inverted
phase contrast microscope. Cell proliferation was detected using
5-bromodeoxyuridine staining. The cytoskeletal protein actin, a
component of focal adhesion plaque protein, vinculin, and the small
GTP-binding proteins RhoA and Rac1 were detected by
immunohistochemistry in the cells located at the margin of and remote
from the wound.
RESULTSThe cells
located at the margin of the wound showed the greatest migration and
proliferation and were found to express more rudimentary lamellipodia
and filopodia in the absence of mechanical strain. Vinculin, RhoA, and
Rac1 were also strongly expressed in the wound margin. Under conditions
of mechanical strain, the speed of migration of cells slowed and fewer
proliferating cells were detected around the wound in a strain strength
dependent manner. Lamellipodial formation, vinculin, RhoA, and Rac1
were poorly expressed in the same area. However, in cells located more than 1 mm from the wound edge, cytoskeletal rearrangement, and the
expression of vinculin, RhoA, and Rac1 were not influenced by
mechanical strain.
CONCLUSIONSMigration
and proliferation of RGM1 cells in culture during wound healing were
inhibited by mechanical strain, which caused dysfunction of the
cytoskeletal and cell adhesion systems. It is suggested that physical
stimulants such as mechanical strain may play a role in gastric wound
healing in vivo by modifying cellular migration and proliferation.
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