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)

Ten consecutive cases of basal cell carcinomas were reviewed. Nine of these displayed the typical histology of basal cell carcinoma, the other case was composed of small spindle to ovoid cells with scant cytoplasm and a high mitotic rate, resembling an "oat cell" carcinoma. These were studied using the immunoperoxidase technique for tissue localization of calcitonin, insulin, glucagon, somatostatin, ACTH, gastrin and nerve growth factor. Three cases were negative for all hormones tested. Three cases were focally positive for a single hormone; one each for calcitonin, somatostatin, and ACTH. Two cases were focally positive for ACTH and somatostatin and two cases were focally positive for calcitonin, somatostatin and ACTH. None of the other hormones displayed activity. The positive staining was eliminated after absorption by the specific antigen. This immunohistochemical study illustrated neuroendocrine differentiation in basal cell carcinomas as has previously been suggested by the Grimelius stain and electron microscopy. Thus, as demonstrated in other epithelial neoplasms, basal cell carcinoma may also display neuroendocrine differentiation. This illustrates the potential multidirectional differentiation in neoplastic epithelial cells.
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PMID:Neuroendocrine differentiation in basal cell carcinomas. 612 Sep 64

In the brain of adult specimens of the tobacco hornworm moth, Manduca sexta (L), cells immunoreactive for several kinds of neuropeptides were localized by means of the PAP procedure, by use of antisera raised against mammalian hormones or hormonal peptides. In contrast, no such neurosecretory cells were found in the corpora cardiaca and corpora allata (CC/CA); in the CC/CA, however, immunoreactive nerve fibres were observed, reaching these organs from the brain. The neurosecretory cells found in the brain were immunoreactive with at least one of the following mammalian antisera, namely those raised against the insulin B-chain, somatostatin, glucagon C-terminal, glucagon N-terminal, pancreatic polypeptide (PP), secretin, vasoactive intestinal polypeptide (VIP), glucose-dependent insulinotropic peptide (GIP), gastrin C-terminus, enkephalin, alpha- and beta-endorphin, Substance P, and calcitonin. No cells were immunoreactive with antisera specific for detecting neurons containing the insulin A-chain, nerve growth factor, epidermal growth factor, insulin connecting peptide (C-peptide), polypeptide YY (PYY), gastrin mid-portion (sequence 6-13), cholecystokinin (CCK) mid-portion (sequences 9-20 and 9-25), neurotensin C-terminus, bombesin, motilin, ACTH, or serotonin. All the neuropeptide-immunoreactive cells observed emitted nerve fibers passing through the brain to the CC and in some cases also to the CA. In CC these immunoreactive nerve fibers tended to accumulate near the aorta. It was speculated that neuropeptides are released into the circulating haemolymph and act as neurohormones.
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PMID:Immunohistochemical investigations of neuropeptides in the brain, corpora cardiaca, and corpora allata of an adult lepidopteran insect, Manduca sexta (L). 613 31

Development of the two putative peptide neurotransmitters, substance P (SP) and somatostatin (SS), were compared in rat dorsal root ganglion (DRG) and spinal cord in vivo. The content of SS in the sixth cervical DRG increased 5-fold during the first 5 weeks of life, rising from 24 pg per ganglion at birth. SP content increased 4.5-fold during the first 5 weeks, from 56 pg per ganglion at birth. The developmental profiles for these two peptides were virtually parallel, suggesting that their respective neuronal populations developed in synchrony. Treatment with nerve growth factor (NGF) significantly increased the content of both SP and SS in the DRG and dorsal spinal cord. Conversely, treatment with capsaicin significantly decreased both SP and SS in the DRG and dorsal spinal cord. Consequently, experiments involving NGF or capsaicin treatment of sensory neurons must be interpreted with extreme care, because specificity is not limited to a single peptide phenotype. Although the mechanisms of action of NGF and capsaicin on SP and SS have not been defined, the similarity of the responses of the two peptides suggests that their development may be regulated by similar processes.
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PMID:Similarities in development of substance P and somatostatin in peripheral sensory neurons: effects of capsaicin and nerve growth factor. 617 69

The protein nerve growth factor (NGF) is a naturally occurring trophic substance for sympathetic neurones and for at least those primary sensory neurones containing substance P (refs 4-6). Thus retrogradely transported NGF increased substance P and protein content in corresponding dorsal root ganglia. Moreover, anti-NGF antibodies administered to newborn rats decreased substance P and somatostatin levels in dorsal root ganglia and dorsal spinal cord, suggesting an important role for NGF in the postnatal development of peptidergic sensory neurones. These neurones appear to be selectively affected by the neurotoxin capsaicin (8-methyl-N-vanillyl-6-nonenamide). Treatment of newborn rats with capsaicin led to degeneration of primary sensory neurones containing substance P, somatostatin, vasoactive intestinal polypeptide and cholecystokinin. The mechanism by which capsaicin evokes its neurotoxic effect is unknown. We report here that in newborn rats concomitant administration of NGF partially antagonized the deleterious effect of capsaicin on substance P-containing neurones in dorsal root ganglia as assessed by morphological and biochemical criteria. We conclude that capsaicin destroys the perikarya of primary sensory peptidergic neurones by interfering with the action of NGF, probably by blocking its retrograde axonal transport.
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PMID:Nerve growth factor antagonizes the neurotoxic action of capsaicin on primary sensory neurones. 618 53

Immunoreactive substance P, somatostatin, gastrin/cholecystokinin and vasoactive intestinal polypeptide were studied in lumbar dorsal root ganglia of 14-day-old rats treated from day 2 to 11 of life with nerve growth factor. Increased staining intensity of neuronal cell bodies and processes for substance P, gastrin/cholecystokinin and vasoactive intestinal polypeptide was observed by immunohistochemistry indicating increased neuronal peptide concentrations. These results were supported by radioimmunoassays showing increased ganglionic levels of substance P and vasoactive intestinal polypeptide. Both techniques, however, failed to show a significant increase of somatostatin levels.
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PMID:Nerve growth factor increases substance P, cholecystokinin and vasoactive intestinal polypeptide immunoreactivities in primary sensory neurones of newborn rats. 619 Dec 53

The frontal ganglion of the adult forms of the tobacco hornworm, Manduca sexta, was investigated immunocytochemically for the occurrence of the gastro-entero-pancreatic (GEP) neurohormonal peptides, namely insulin, nerve growth factor, epidermal growth factor, insulin C-peptide, somatostatin, glucagon, glicentin, pancreatic polypeptide (PP), polypeptide YY (PYY), secretin, vasoactive intestinal peptide (VIP), gastric inhibitory peptide (GIP), gastrin, cholecystokinin (CCK), enkephalin, alpha- and beta-endorphins, substance P, neurotensin, bombesin, motilin, ACTH, serotonin, and calcitonin. Among all the antisera tested, positive immunostaining was obtained with anti-insulin B-chain serum only. The insulin B-chain immunoreactivity was localized in 4-6 large (30-40 microns) neurons, in the neuropile, and in the recurrent nerve. It is speculated that the insulin-like immunoreactive material may be transported to the neurohaemal organ (corpora cardiaca) through the nervi cardiaco-somatogastrici.
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PMID:Immunocytochemical evidence for the occurrence of insulin in the frontal ganglion of a Lepidopteran insect, the tobacco hornworm moth, Manduca sexta L. 637 93

The importance of nerve growth factor (NGF) for the development of sensory ganglia was investigated by injecting rat fetuses (16.50 days of gestation) with a single dose of anti-NGF antiserum. Four months later the treated animals showed a very large decrease in substance P- and somatostatin-like immunoreactivities in dorsal root ganglia and skin with a lesser decrease in trigeminal ganglia. Fluoride-resistant acid phosphatase, substance P-, and somatostatin-like immunoreactivities were greatly decreased in the dorsal horn of the spinal cord. No change in neurotensin- and [Met]enkephalin-like immunoreactivities was observed. The anti-NGF antiserum treatment produced a greater than 90% decrease in the number of unmyelinated dorsal root fibers and a 35% decrease in the total number of myelinated fibers. The loss in myelinated fibers was restricted to small-diameter fibers with no change in large-diameter fibers. No change in taste bud morphology was noted, thereby refuting the proposal that anti-NGF antiserum treatment may represent an animal model for familial dysautonomia. The present results indicate that NGF is a necessary requirement for the normal development of a significant population of prenatal rat dorsal root ganglion cells.
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PMID:Biochemical and anatomical effects of antibodies against nerve growth factor on developing rat sensory ganglia. 660 28

In this minireview we will discuss some evidence suggesting that the immune response is under neuronal regulation. In particular, we will concentrate on the effects that various neuropeptides have on immunity both in vitro and in vivo. Of these, vasoactive intestinal peptide, substance P, somatostatin, and calcitonin gene related peptide will be discussed in detail. In addition, the effects of nerve growth factor on the immune system will be presented. Finally, a possible role for these neuropeptides in various diseases and its clinical relevance will be suggested.
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PMID:Neuronal factors modulating immunity. 748 36

Adult rat dorsal root ganglion sensory neurons in culture require nerve growth factor for synthesis of substance P and calcitonin gene-related peptide but express vasoactive intestinal peptide independently of nerve growth factor. In contrast, the same neurons from newborn rats do not express detectable vasoactive intestinal polypeptide when cultured with nerve growth factor. To further explore the mechanisms regulating neuropeptide expression in these cells, I compared the effects of nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3, ciliary neurotrophic factor and leukaemia inhibitory factor on substance P, calcitonin gene-related peptide, vasoactive intestinal polypeptide and somatostatin expression in rat dorsal root ganglion cultures. As with neurons from adult animals, newborn rat sensory neurons required nerve growth factor for synthesis of substance P and calcitonin gene-related peptide. This effect was independent of neuronal survival since most neurons capable of expressing these peptides appeared to survive without added neurotrophic factors. Neurons surviving in the absence of nerve growth factor also expressed vasoactive intestinal polypeptide, suggesting that nerve growth factor suppresses vasoactive intestinal polypeptide expression in immature neurons. However, nerve growth factor withdrawal after eight days' culture failed to cause vasoactive intestinal polypeptide induction which therefore appears to depend on other factors also. Neither ciliary neurotrophic factor nor leukaemia inhibitory factor affected peptide levels when used alone, but both inhibited nerve growth factor-stimulated expression of substance P and calcitonin gene-related peptide in adult rat neurons. They also stimulated vasoactive intestinal polypeptide expression in newborn rat neurons in the presence of nerve growth factor but not to such high levels as those seen under conditions of nerve growth factor deprivation. Neither brain-derived neurotrophic factor nor neurotrophin-3 affected peptide expression significantly. Somatostatin was defected in adult rat neurons, but was unaffected by neurotrophic factors. No somatostatin was detected in newborn rat neurons. These results suggest that in immature animals at least, the increased expression of vasoactive intestinal polypeptide seen in sensory neurons following peripheral nerve injury in vivo, could result from deprivation of target-derived nerve growth factor in combination with increased availability of ciliary neurotrophic factor or leukaemia inhibitory factor from the injured nerve.
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PMID:Neuropeptide expression by newborn and adult rat sensory neurons in culture: effects of nerve growth factor and other neurotrophic factors. 751 8

The expression of three enteric neuropeptides was examined in freshly dispersed ganglia and in ganglia cultured for up to 28 days. During culture, glial cells grew into a flat sheet surrounding a cluster of neurons identified with neuron-specific enolase (13 +/- 2/ganglion), which remained constant throughout the period of culture. The neurons underwent a distinctive temporal change, resulting in overexpression of substance P (SP), normal expression of somatostatin, and virtual suppression of vasoactive intestinal peptide (VIP). Three weeks after the start of culture, the ganglia contained and released (in response to 55 nM KCl, 0.1 mM 1,1-dimethyl-4-phenylpiperazinium, or 1 microM gastrin-releasing peptide) twice as much SP as freshly dispersed ganglia, corresponding to a sevenfold increase per cultured neuron; content and release of somatostatin did not change. SP content and release declined to 1.5% of those found in control cultures when nonneuronal cells were suppressed with cytosine arabinoside but were partially restored (13-17% of control) by nerve growth factor. In marked contrast, VIP was minimally (< 1%) present in and released from ganglia after the third day in culture. Suppression of VIP could reflect a selective loss of VIP neurons and/or VIP expression.
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PMID:Differential expression of substance P, somatostatin, and VIP in neurons from cultured myenteric ganglia. 752 Nov 37


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