title: 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.
abstract: 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.
authors: Third Department of Internal Medicine, University of Occupational and Environmental Health, Japan, School of Medicine, Kitakyushu, Fukuoka, Japan. hayaton@med.uoeh-u.ac.jp
authors: Hayato
authors: H
authors: Nakamura
authors: Mitsuo
authors: M
authors: Tashiro
authors: Taizo
authors: T
authors: Yamaguchi
authors: Hiroshi
authors: H
authors: Asaumi
authors: Yoko
authors: Y
authors: Nomiyama
authors: Shiro
authors: S
authors: Watanabe
authors: Yoshikuni
authors: Y
authors: Nagashio
authors: Tamao
authors: T
authors: Miyamoto
authors: Makoto
authors: M
authors: Otsuki
mesh_terms: 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
chemical_list: 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