Relationship between polyamines, actin distribution, and gastric
healing in rats.
Banan, Ali, Jian-Ying Wang, Shirley A. McCormack, and Leonard R.
Johnson.
Department of Physiology and Biophysics, The University of
Tennessee College of Medicine, Memphis, Tennessee 38163
APStracts 3:0127G, 1996.
Intragastric administration of 3.4 M NaCl damages the gastric mucosa
and increases the activity of ornithine decarboxylase (ODC), the rate
limiting enzyme in polyamine synthesis. Polyamines are essential for
the repair of gastric erosions. Little is known about the restitution
of damaged mucosa except that cell migration is essential. Actin is
the principal cytoskeletal protein and is essential for migration.
This investigation determines the relationship between polyamines,
actin, and gastric healing. Rats were fasted for 22 h and given 1.0
ml of 3.4 M NaCl intragastrically and killed 1, 2, 4, 8, and 10 h
later. The mucosa was assayed for ODC activity, and stained for G-and
F-actin. F-actin was concentrated below the damaged mucosa at 1.5, 2,
and 4 h. There was no increase in F-actin distribution at any time
point, when NaCl treated animals were given [alpha]
-difluoromethylornithine, a specific inhibitor of ODC. In addition,
DFMO significantly prevented the healing of the mucosal lesions.
Spermidine treatment following DFMO+NaCl significantly prevented the
effects of DFMO. Cytochalasin-D, a potent actin disrupting drug,
significantly delayed normal gastric mucosal healing. The endogenous
polyamines increased significantly in NaCl animals. Data indicate
that increases in polyamine synthesis following damage influence the
distribution of F-actin in vivo, which may play a part in the healing
of mucosal erosions.
Received 26 July 1995; accepted in final form 10 June 1996.
APS Manuscript Number G318-5.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 4 July 96