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F Müller-Pillasch

Publications and source records attributed to F Müller-Pillasch.

21 records · Page 2Linked to original sources
PubMed1994

Enhancement of transforming growth factor beta 1 expression in the rat pancreas during regeneration from caerulein-induced pancreatitis.

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 beta 1 (TGF beta 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 0 h, 12 h, 24 h, 2, 3 and 7 days after induction of caerulein pancreatitis. Transcript levels for TGF beta 1 were measured by slot-blot analysis and mRNA in situ hybridization. Total amount of TGF beta 1-protein was measured using a radioligand binding assay. TGF beta 1 protein was increased twofold after 24 h and 48 h and returned to control values 7 days after induction of pancreatitis, TGF beta 1-mRNA reached maximal values (3-fold over controls) after 2 days. The largest amount of TGF beta 1-mRNA was found in pancreatic acinar cells and in stromal cells. In summary, expression of TGF beta 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 beta 1 in the regulation of extracellular matrix regeneration in the rat pancreas after caerulein-induced pancreatitis.

Animals↗
PubMed1994

Balance of expression of genes coding for extracellular matrix proteins and extracellular matrix degrading proteases in chronic pancreatitis.

Chronic pancreatitis is characterized by proliferation of the extracellular matrix and by increased deposition of interstitial extracellular matrix proteins (collagens type I and III, fibronectin). In this study we analyzed the balance of expression of mRNAs encoding extracellular matrix components (collagens I, III and IV, laminin, fibronectin), extracellular matrix degrading metalloproteinases (MMP-1, -2 and -3) and tissue inhibitors of metalloproteinases (TIMP-1 and -2) in chronic pancreatitis (n = 8) and control pancreas (n = 7) by northern blot analysis. Transcripts for MMP-1 (interstitial collagenase), MMP-3 (stromelysin) and TIMP-1 were not detectable in chronic pancreatitis and control tissues. Steady-state levels of transcripts encoding extracellular matrix proteins, MMP-2 (72 kDa collagenase IV) and TIMP-2 were enhanced in 7 out of 8 chronic pancreatitis tissue samples and showed a large degree of variation between individual patients. Transcript levels could not be correlated to the histologically detectable degree of inflammation and fibrosis or to the total amount of deposited collagen protein, which was high in all chronic pancreatitis tissue samples as determined by a standard colorimetric procedure. Increased steady state levels of transcripts encoding extracellular matrix proteins or extracellular matrix degrading proteases may thus reflect the activity of processes involved in the remodeling of the gland during chronic inflammation. The precise role of overexpression of MMP-2 and its inhibitor TIMP-2 will have to be elucidated in further studies.

Chronic Disease↗