Kallikrein-gene expression in the rat gastrointestinal tract

Abstract

The serine proteinase glandular kallikrein has been demonstrated in the gastrointestinal tract, although there is some doubt as to whether it is synthesized there or derives from exocrine-gland secretions. Using a rat pancreatic kallikrein cRNA probe we have demonstrated kallikrein-like gene expression in the corpus, duodenum, jejunum, ileum, caecum and colon, and compared the pattern of expression with that of the gastrointestinal peptides somatostatin, gastrin and glucagon. In addition, using a panel of oligonucleotide probes specific for various members of the rat kallikrein-gene family, we have shown that the kallikrein-like gene expressed appears to be expressed as true kallikrein.

Change in Annexin A3 Expression by Regulatory Factors of Hepatocyte Growth in Primary Cultured Rat Hepatocytes

“…For example, Dex and other glucocorticoids stimulate AnxA1 expression in vitro [28][29][30][31][32] and in vivo, [33][34][35][36] in contrast to the present finding. This inconsistency suggests that the mode of regulation by glucocorticoids differs among species of Anxs, tissues, and cells.…”

Lipocortin 1 mediates dexamethasone-induced growth arrest of the A549 lung adenocarcinoma cell line.

“…Fig. 6 (29,31), rat macrophages and thymus in vivo (32,33), and human bronchoalveolar lavage fluid (34). Some undifferentiated cells in culture do not respond to glucocorticoids with an induction of lipocortin 1 (35), but induction can occur once the cells are differentiated (36).…”

Dexamethasone Alters Arachidonate Release from Human Epithelial Cells by Induction of p11 Protein Synthesis and Inhibition of Phospholipase A2 Activity

“…A group of structurally related, calcium-dependent phospholipid-binding proteins, annexins, which were formerly known as lipocortins or calpactins, had been shown to be inducible by glucocorticoids. Annexin I has been reported to inhibit sPLA 2 activity in vitro (25)(26)(27)(28)(29)(30). These observations led to the hypothesis that the inhibition of sPLA 2 by annexins is the mechanism of the anti-inflammatory action of glucocorticoids.…”

“…The decreased synthesis of bioactive eicosanoids may represent an important mechanism of the antiinflammatory action of glucocorticoids. Glucocorticoids can induce annexins which might inhibit sPLA 2 activity in vitro (25)(26)(27)(28)(29)(30). A recent study has demonstrated that p11 can directly interact with the COOH-terminal region of 85-kDa cPLA 2 and inhibit cPLA 2 enzyme activity (31).…”