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Enhancement of transforming growth factor β 1 expression in the rat pancreas during regeneration from caerulein‐induced pancreatitis
Author(s) -
GRESS T.,
MÜLLERPILLASCH F.,
ELSÄSSER H.P.,
BACHEM M.,
FERRARA C.,
WEIDENBACH H.,
LERCH M.,
ADLER G.
Publication year - 1994
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1994.tb01060.x
Subject(s) - stromal cell , pancreas , acinar cell , pancreatitis , medicine , extracellular matrix , northern blot , endocrinology , transforming growth factor beta , transforming growth factor , ceruletide , messenger rna , extracellular , biology , cholecystokinin , microbiology and biotechnology , gene , biochemistry , receptor
Synthesis of extracellular matrix components is enhanced in the rat pancreas during regeneration from caerulein‐induced pancreatitis. To study the involvement of transforming growth factor β 1 (TGF β 1), one of the most potent modulators of the extracellular matrix, in the process of pancreatic regeneration we examined the expression of this gene on the transcript and protein level. Pancreatic RNA was extracted from rats killed 0h, 12h, 24h, 2, 3 and 7 days after induction of caerulein pancreatitis. Transcript levels for TGF β 1 were measured by slot–blot analysis and mRNA in situ hybridization. Total amount of TGF β 1‐protein was measured using a radioligand binding assay. TGF β 1 protein was increased twofold after 24h and 48h and returned to control values 7 days after induction of pancreatitis, TGF β 1‐mRNA reached maximal values (3‐fold over controls) after 2 days. The largest amount of TGF β 1‐mRNA was found in pancreatic acinar cells and in stromal cells. In summary, expression of TGF β 1 in acinar and stromal cells of the rat pancreas is enhanced during regeneration from caerulein‐induced pancreatitis, which may indicate an involvement of TGF β 1 in the regulation of extracellular matrix regeneration in the rat pancreas after caerulein‐induced pancreatitis.