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

Somatostatin analogue octreotide inhibits intestinal absorption and motility but its effect on epithelial cell migration and proliferation remains unclear. Our aim was to determine the effect of octreotide on parameters of intestinal regeneration, including epidermal growth factor (EGF)-induced changes. Thirty rabbits had full-thickness ileal defects patched with cecal serosa surface. Group 1 were controls. Groups 2 and 3 received 100 micrograms and 1000 micrograms, respectively, of subcutaneous octreotide daily. Group 4 received EGF at 1.5 micrograms/kg per hour via subcutaneous miniosmotic pump, and group 5 received both octreotide (1000 micrograms/d) and EGF (1.5 micrograms/kg per hour). Octreotide at 100 micrograms/d did not inhibit epithelial cell migration or proliferation at 7 days. Octreotide at 1000 micrograms/d inhibited normal but not EGF-stimulated cell migration. Octreotide decreased EGF-stimulated but not normal proliferation. Octreotide impairs epithelial cell migration in a dose-dependent manner. Octreotide inhibits EGF-stimulated proliferative activity but not EGF-stimulated migration. Prolonged administration of octreotide may adversely affect normal and adaptive intestinal regeneration by both direct and indirect effects.
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PMID:Somatostatin analogue inhibits intestinal regeneration. 845 51

The somatostatin analogue octreotide impairs intestinal regeneration and the adaptive response to intestinal resection and other stimuli. These effects are mediated in part by inhibition of enterocyte migration and proliferation. The aim of this study was to determine whether octreotide promotes enterocyte apoptosis. Twenty-four New Zealand white rabbits were studied including 18 animals that underwent patch enteroplasty in the distal ileum to stimulate the mucosa and six unoperated controls. The patched animals either received 100 microgram or 1000 microgram of subcutaneous octreotide daily or served as operated control subjects. Normal ileal mucosa adjacent to the patch was evaluated at 7 days for villus height, crypt depth, crypt cell production rate (CCPR), and in situ end labeling of DNA fragmentation. Mean DNA fragmentation was significantly greater in octreotide-treated animals (P <0.05 Mann-Whitney rank test). Fragmentation scores ranged from 1.0 to 1.5 in controls and 1.1 to 2. 65 in treated animals. Staining of enterocytes was quite heterogenous, however, among the villi of individual treated animals. Staining was greater and cells with chromatin condensation were more prevalent near the tip of the villus. Octreotide increased apoptosis at the villus tip, lateral villus, and crypt. The two control groups had similar villus height, crypt depth, and CCPR The two octreotide-treated groups had similar villus height and CCPR compared to control animals. However, crypt depth was significantly less in the octreotide-treated animals (100 +/- 9 micrometer and 90 +/- 6 micrometer, 100 microgram, and 1000 microgram) compared to controls (121 +/- 10 micrometer and 117 +/- 10 micrometer, unoperated and operated; P <0.05). Crypt depth but not villus height correlated with DNA fragmentation. Neither correlated with CCPR. The following conclusions were reached: (1) Octreotide treatment is associated with increased DNA fragmentation in enterocytes; (2) octreotide promotes apoptosis in both villus and crypt compartments; (3) predisposition to apoptosis may play a role in octreotides effects on intestinal regeneration and adaptation; and (4) the role of proliferation and apoptosis in determining the size of the enterocyte compartments remains unclear.
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PMID:Somatostatin analogue predisposes enterocytes to apoptosis. 983 14

The definition of neurotransmitter receptors expressed by individual neuronal phenotypes is essential for our understanding of integrated neural regulation. We report here a single-neuron strategy using green fluorescent protein (GFP)-promoter transgenic mice and oligonucleotide microarrays that has enabled us to provide a qualitative profile of the neurotransmitter receptors expressed by the gonadotropin- releasing hormone (GnRH) neurons, critical for the neural regulation of fertility. Acute brain slices were prepared from adult female GnRH-GFP transgenic mice and single GnRH neurons identified and patched. The contents of GnRH neurons underwent reverse transcription and cDNA amplification using the switch mechanism at the 5' end of RNA templates system, and hybridization to mouse gene oligonucleotide arrays. Fifty different neurotransmitter receptor subunit mRNAs were detected in GnRH neurons. Many of the classical amino acid and aminergic receptors were present in addition to 14 distinct, and in most cases novel, neuropeptidergic receptor signaling families. Four of the latter were selected for functional validation with gramicidin-perforated patch-clamp electrophysiology. Galanin, GnRH and neuromedin B were all found to exert direct depolarizing actions upon GnRH neurons whereas somatostatin induced a potent hyperpolarizing response. These studies demonstrate a relatively straightforward approach for transcriptome profiling of specific neuronal phenotypes. The stimulatory actions of GnRH and galanin upon GnRH neurons found here indicate that positive ultrashort feedback loops exist among the GnRH neuronal population.
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PMID:Profiling neurotransmitter receptor expression in mouse gonadotropin-releasing hormone neurons using green fluorescent protein-promoter transgenics and microarrays. 1583 32