Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Phenol red, which is commonly used in culture media as a pH indicator, has recently been shown to possess estrogenic properties. In this study we investigated the effects of phenol red on prolactin release and synthesis by cultured female and male rat anterior pituitary cells and on the sensitivity of these cells of dopamine, TRH and somatostatin (SRIF). It was shown that phenol red stimulated rat prolactin release and cell content in a dose-dependent manner. The effects of 30 microM phenol red, which is the medium concentration in our regular culture medium, and a submaximally active concentration of 17 beta-estradiol (E2) were additive. Male rat pituitary cells were far more responsive to phenol red and also to E2 than female pituitary cells. The antiestrogen tamoxifen (100 nM) significantly inhibited the phenol red-stimulated prolactin release by male rat pituitary cells but caused a 2-fold increase of prolactin release in the absence of phenol red. 30 microM phenol red did not modulate the responsiveness of female and male rat lactotrophs to dopamine, TRH or SRIF. We propose from our results that the estrogenic effect of 30 microM phenol red is too weak in order to alter the responsiveness of rat lactotrophs to dopamine, TRH and SRIF but the presence of phenol red in culture media should be considered when the effects of estrogens and antiestrogens on rat prolactin release and synthesis in vitro are studied.
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PMID:Weak estrogenic activity of phenol red in the culture medium: its role in the study of the regulation of prolactin release in vitro. 289 May 43

Peptide-23 is a 16-kilodalton protein secreted by rat pituitary cells that was first identified because it was regulated by GRF and somatostatin in a similar fashion to GH. Cloning of peptide-23 complementary DNA revealed that it is identical to pancreatitis-associated protein (PAP) and a member of the c-lectin gene family. We examined the expression of peptide-23/PAP and a structurally related protein, pancreatic stone protein (PSP/reg), in the rat gastrointestinal tract. Here we report age-related changes in the expression and GRF regulation of peptide-23. Both peptide-23/PAP messenger RNA (mRNA) and PSP/reg mRNA were virtually undetectable in the small intestine of newborn and 1- and 2-week-old rats. A dramatic increase in the expression of both genes was seen at the time of weaning in the third week postpartum. The abundance of both of these mRNA decreases after 3 and 6 months of age. Peptide-23/PAP mRNA is most abundant in the ileum, whereas PSP/reg is maximally expressed in the pancreas and duodenum. Human GRF analog pellets were implanted sc into adult male rats for 2 weeks to study the chronic effects of GRF on the expression of these genes. Both peptide-23/PAP and PSP/reg mRNA levels in duodenum and jejunum were increased in these rats compared with levels in control rats. However, no increase in peptide-23/PAP mRNA in response to GRF treatment was seen in the ileum, where the level of expression of this gene is very high, and GRF had no effect on peptide-23/PSP expression in the heart, pituitary, or hypothalamus, where expression is normally undetectable. In situ hybridization was used to localize peptide-23/PSP in the small intestine and pancreas of GRF-treated rats. An increase in peptide-23/PAP mRNA was restricted to acinar cells close to islets, whereas little expression was seen in acinar cells distant from islets, suggesting that either peptide-23/PAP may have some paracrine action on the islets, or alternatively, an islet-derived factor may function as a paracrine modulator of peptide-23/PAP expression. These data demonstrate that GRF modulates peptide-23/PAP expression in the gastrointestinal tract in a similar fashion to that previously reported for pituitary cells in primary culture.
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PMID:Age-related changes in peptide-23/pancreatitis-associated protein and pancreatic stone protein/reg gene expression in the rat and regulation by growth hormone-releasing hormone. 772 Jun 28

PSP is associated with a widespread cholinergic deficit likely corresponding to a loss in cholinergic neurons. The cholinergic damage dramatically affects the basal ganglia and specific cell groups of the mesencephalon and pons. This provides an anatomically defined basis for motor and supranuclear oculomotor syndromes characteristic of PSP. Unlike Alzheimer's disease and Parkinson's disease with dementia, the disease is not associated with a marked cholinergic deficiency in the cerebral cortex. Various peptides are present at normal concentrations in extrapyramidal and limbic subcortical areas in brains of patients with PSP. Of particular interest, is somatostatin, the levels of which are subnormal in cerebral cortex of patients with dementia of Alzheimer' or Parkinson's disease type.
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PMID:Cholinergic and peptidergic systems in PSP. 796 88