Preferential increase of extracellular matrix expression relative to transforming growth factor beta1 in the pancreas during the early stage of acute hemorrhagic pancreatitis in rats.
OBJECTIVE
To elucidate the role of transforming growth factor (TGF) beta1 and extracellular matrix (ECM) after acute necrotizing pancreatitis, we studied the regulation of TGF-beta1 and ECM after induction of pancreatitis.


METHODS
We examined the serial changes of levels of plasma TGF-beta1 by enzyme-linked immunoassay and expression of TGF-beta1 and ECM by Northern and Western blot analyses, respectively, in the pancreas after induction of sodium taurocholate-induced acute pancreatitis.


RESULTS
Plasma total (active and inactive) TGF-beta1 levels at 3 hours after induction of pancreatitis were significantly increased compared with baseline values. The levels of TGF-beta1 messenger RNA (mRNA) were unaltered by day 2. Levels of fibronectin mRNA at 3 hours after induction of pancreatitis were already higher than the baseline values. Latency-associated peptide-TGF-beta1 showed a peak on day 7. Thus, the expression of ECM mRNA increased earlier than that of TGF-beta1 mRNA.


CONCLUSIONS
These results suggest that the increase in plasma TGF-beta1 concentration probably results from the elevated secretion of TGF-beta1 from several cells and/or the redistribution of TGF-beta1 protein and that the increase in expression of ECM probably is associated with the activation of TGF-beta1. It is conceivable that both increased plasma concentration and focal activation of TGF-beta1 play an important role in ECM production during the early stage of acute pancreatitis.
Nakamura
Hayato
H
Third Department of Internal Medicine, University of Occupational and Environmental Health, Japan, School of Medicine, Kitakyushu, Fukuoka, Japan. hayaton@med.uoeh-u.ac.jp
Tashiro
Mitsuo
M
Yamaguchi
Taizo
T
Asaumi
Hiroshi
H
Nomiyama
Yoko
Y
Watanabe
Shiro
S
Nagashio
Yoshikuni
Y
Miyamoto
Tamao
T
Otsuki
Makoto
M
D000208:Acute Disease; D000818:Animals; D024042:Collagen Type I / Q000378:metabolism; D024141:Collagen Type IV / Q000378:metabolism; D004195:Disease Models, Animal; D016326:Extracellular Matrix Proteins / Q000235:genetics / Q000378:metabolism*; D005353:Fibronectins / Q000378:metabolism; D006470:Hemorrhage / Q000097:blood / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D008297:Male; D010179:Pancreas / Q000378:metabolism* / Q000473:pathology; D010195:Pancreatitis / Q000097:blood / Q000139:chemically induced / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D011347:Procollagen / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013656:Taurocholic Acid; D013997:Time Factors; D053773:Transforming Growth Factor beta1 / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D015854:Up-Regulation
D024042:Collagen Type I; D024141:Collagen Type IV; D016326:Extracellular Matrix Proteins; D005353:Fibronectins; D011347:Procollagen; D012333:RNA, Messenger; D053773:Transforming Growth Factor beta1; D013656:Taurocholic Acid