Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Parenterally administered substance P suppressed stress-induced eating (resulting from mild tail pinch) in a dose-related manner, whereas at similar or higher doses of substance P starvation-induced eating was uneffected. This specific effect of substance P on stress-induced eating is possibly associated with alterations of exogenous substance P of the normal modulation of pain transmission.
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PMID:Substance P suppresses stress-induced eating. 616 30

Substance P (SP) was recognized to stimulate cell growth. The mechanisms of growth control by SP are unknown. We, therefore, investigated mechanisms of the effect of SP on proliferation of human skin fibroblasts. SP did not stimulate proliferation of fibroblasts growth arrested by serum starvation over 48 hours. However, in the presence of acetylsalicylic acid SP potently stimulated fibroblast growth. A bell-shaped dose-response curve with maximal stimulation at picomolar concentrations was found. Specificity of the mitogenic effect was analyzed by use of synthetic SP analogs. Only neurokinin-1 receptor agonists were active, whereas a specific neurokinin-2 receptor analog did not exhibit mitogenicity. Analyzing the supernatants of growth-arrested fibroblasts treated with SP indicated that SP provokes release of the arachidonic acid metabolites, prostaglandin E2, and prostacyclin but not thromboxane B2 or leukotriene B4. Since similar response patterns in proliferation and arachidonic acid metabolite release have been described for several proinflammatory cytokines, some of which are known to act as competence factors in proliferation, we characterized the mitogenic effect of SP. Results established that SP stimulates fibroblast growth in a manner typical of competence factors. We conclude that arachidonic acid metabolites are involved in the cell cycle-dependent mitogenic action of SP on human skin fibroblasts.
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PMID:Substance P: a competence factor for human fibroblast proliferation that induces the release of growth-regulatory arachidonic acid metabolites. 768 72

The effect of starvation on allergen-induced skin wheal responses and plasma neuropeptide levels was not previously reported. Starvation for 24 h reduces allergen-induced skin wheal responses and plasma levels of substance P and vasoactive intestinal peptide in patients with atopic eczema/dermatitis syndrome, but not in control subjects. These results may have implications for the pathophysiology of the atopic eczema/dermatitis syndrome.
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PMID:Starvation reduces allergen-induced skin wheal responses and plasma substance P and vasoactive intestinal peptide in patients with atopic eczema/dermatitis syndrome. 1240 28

A number of evidences suggest that tachykinin-related peptides (TRPs) of insects can stimulate food consumption after being released from the midgut to the hemolymph. The idea of the present work has been to test this hypothesis in the anautogenous cockroach Blattella germanica. First, we have identified the peptide LemTRP-1 (APSGFLGVR-NH(2)) from brain extracts, by means of an ELISA developed with a polyclonal antibody against this peptide. ELISA studies have also shown that, whereas brain LemTRP-1 levels were fairly constant, midgut levels increase to a maximum on day 3 after adult emergence, falling thereafter until the end of the gonadotrophic cycle. Interestingly, maximum values of food consumption are concomitant with the decrease of LemTRP-1 immunoreactivity in the midgut. Furthermore, starvation decreases LemTRP-1 immunoreactivity in midgut, whereas in the hemolymph it increases. Finally, injection of synthetic LemTRP-1 to adult females significantly stimulates food consumption. The whole observations suggest that LemTRP-1 is released from the midgut to the hemolymph when sustained food consumption is required to maintain vitellogenesis at the highest levels, and that LemTRP-1 in the hemolymph stimulates food consumption in these days.
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PMID:Identification of a tachykinin-related peptide with orexigenic properties in the German cockroach. 1817 89

In Drosophila, neurosecretory cells that release peptide hormones play a prominent role in the regulation of development, growth, metabolism, and reproduction. Several types of peptidergic neurosecretory cells have been identified in the brain of Drosophila with release sites in the corpora cardiaca and anterior aorta. We show here that in adult flies the products of three neuropeptide precursors are colocalized in five pairs of large protocerebral neurosecretory cells in two clusters (designated ipc-1 and ipc-2a): Drosophila tachykinin (DTK), short neuropeptide F (sNPF) and ion transport peptide (ITP). These peptides were detected by immunocytochemistry in combination with GFP expression driven by the enhancer trap Gal4 lines c929 and Kurs-6, both of which are expressed in ipc-1 and 2a cells. This mix of colocalized peptides with seemingly unrelated functions is intriguing and prompted us to initiate analysis of the function of the ten neurosecretory cells. We investigated the role of peptide signaling from large ipc-1 and 2a cells in stress responses by monitoring the effect of starvation and desiccation in flies with levels of DTK or sNPF diminished by RNA interference. Using the Gal4-UAS system we targeted the peptide knockdown specifically to ipc-1 and 2a cells with the c929 and Kurs-6 drivers. Flies with reduced DTK or sNPF levels in these cells displayed decreased survival time at desiccation and starvation, as well as increased water loss at desiccation. Our data suggest that homeostasis during metabolic stress requires intact peptide signaling by ipc-1 and 2a neurosecretory cells.
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PMID:Metabolic stress responses in Drosophila are modulated by brain neurosecretory cells that produce multiple neuropeptides. 2062 3

Drosophila insulin-like peptides (DILPs) play important hormonal roles in the regulation of metabolic carbohydrates and lipids, but also in reproduction, growth, stress resistance and aging. In spite of intense studies of insulin signaling in Drosophilag the regulation of DILP production and release in adult fruit flies is poorly understood. Here we investigated the role of Drosophila tachykinin-related peptides (DTKs) and their receptors, DTKR and NKD, in the regulation of brain insulin-producing cells (IPCs) and aspects of DILP signaling. First, we show DTK-immunoreactive axon terminations close to the presumed dendrites of the IPCs, and DTKR immunolabeling in these cells. Second, we utilized targeted RNA interference to knock down expression of the DTK receptor, DTKR, in IPCs and monitored the effects on Dilp transcript levels in the brains of fed and starved flies. Dilp2 and Dilp3, but not Dilp5, transcripts were significantly affected by DTKR knockdown in IPCs, both in fed and starved flies. Both Dilp2 and Dilp3 transcripts increased in fed flies with DTKR diminished in IPCs whereas at starvation the Dilp3 transcript plummeted and Dilp2 increased. We also measured trehalose and lipid levels as well as survival in transgene flies at starvation. Knockdown of DTKR in IPCs leads to increased lifespan and a faster decrease of trehalose at starvation but has no significant effect on lipid levels. Finally, we targeted the IPCs with RNAi or ectopic expression of the other DTK receptor, NKD, but found no effect on survival at starvation. Our results suggest that DTK signaling, via DTKR, regulates the brain IPCs.
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PMID:Regulation of insulin-producing cells in the adult Drosophila brain via the tachykinin peptide receptor DTKR. 2211 63

Macronutrients are essential elements for plant growth and development. In natural, non-cultivated systems, the availability of macronutrients is not a limiting factor of growth, due to fast recycling mechanisms. However, their availability might be an issue in modern agricultural practices, since soil has been frequently over exploited. From a crop management perspective, the nitrogen (N), phosphorus (P), and potassium (K) are three important limiting factors and therefore frequently added as fertilizers. NPK are among the nutrients that have been reported to alter post-embryonic root developmental processes and consequently, impairs crop yield. To cope with nutrients scarcity, plants have evolved several mechanisms involved in metabolic, physiological, and developmental adaptations. In this scenario, microRNAs (miRNAs) have emerged as additional key regulators of nutrients uptake and assimilation. Some studies have demonstrated the intrinsic relation between miRNAs and their targets, and how they can modulate plants to deal with the NPK availability. In this review, we focus on miRNAs and their regulation of targets involved in NPK metabolism. In general, NPK starvation is related with miRNAs that are involved in root-architectural changes and uptake activity modulation. We further show that several miRNAs were discovered to be involved in plant-microbe symbiosis during N and P uptake, and in this way we present a global view of some studies that were conducted in the last years. The integration of current knowledge about miRNA-NPK signaling may help future studies to focus in good candidates genes for the development of important tools for plant nutritional breeding.
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PMID:NPK macronutrients and microRNA homeostasis. 2613 63

Dimorphic plant species can show distinct nutrient needs due to sex-related differences in nutrient allocation to reproductive structures, which can potentially affect their sensitivity to photoinhibition and photo-oxidative stress. Here, we investigated sex-related differences in the extent of photo-oxidative stress in male and female individuals of U. dioica exposed to a combination of severe drought and nutrient starvation. Male and female individuals of U. dioica subject to severe drought stress were exposed to various levels of nutrient availability. First, a set of plants grown under field conditions and exposed to summer drought was used to test the effects of nutrient supply (given as NPK fertilizer). Secondly, the effects of various phosphate concentrations in the nutrient solution were tested in drought-stressed potted plants. The Fv/Fm ratio (maximum efficiency of PSII photochemistry), photoprotection capacity (levels of carotenoids, including the xanthophyll cycle, and vitamins C and E), and the extent of lipid peroxidation (hydroperoxide levels) were measured. Results showed that an application of the NPK fertilizer to the soil had a positive effect on drought-stressed plants, reducing the extent of lipid peroxidation in both males and females. P deficiency led to residual photoinhibition, as indicated by significant reductions in the Fv/Fm ratio, and enhanced lipid peroxidation in females, but not in males. We conclude that (i) increased nutrient availability in the soil can alleviate photo-oxidative stress in drought-stressed U. dioica plants, and (ii) U. dioica plants show sexual secondary dimorphism in terms of photoinhibition and photo-oxidative stress, but this is only apparent when stress infringed on plants is very severe.
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PMID:Sex-related differences in photoinhibition, photo-oxidative stress and photoprotection in stinging nettle (Urtica dioica L.) exposed to drought and nutrient deficiency. 2679 30

The intestine is involved in digestion and absorption, as well as the regulation of metabolism upon sensation of the internal intestinal environment. Enteroendocrine cells are thought to mediate these internal intestinal chemosensory functions. Using the CaLexA (calcium-dependent nuclear import of LexA) method, we examined the enteroendocrine cell populations that are activated when flies are subjected to various dietary conditions such as starvation, sugar, high fat, protein, or pathogen exposure. We find that a specific subpopulation of enteroendocrine cells in the posterior midgut which express Dh31 and tachykinin are activated by the presence of proteins and amino acids.
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PMID:A subset of enteroendocrine cells is activated by amino acids in the Drosophila midgut. 2680 53

Dysregulation of sleep or feeding has enormous health consequences. In humans, acute sleep loss is associated with increased appetite and insulin insensitivity, while chronically sleep-deprived individuals are more likely to develop obesity, metabolic syndrome, type II diabetes, and cardiovascular disease. Conversely, metabolic state potently modulates sleep and circadian behavior; yet, the molecular basis for sleep-metabolism interactions remains poorly understood. Here, we describe the identification of translin (trsn), a highly conserved RNA/DNA binding protein, as essential for starvation-induced sleep suppression. Strikingly, trsn does not appear to regulate energy stores, free glucose levels, or feeding behavior suggesting the sleep phenotype of trsn mutant flies is not a consequence of general metabolic dysfunction or blunted response to starvation. While broadly expressed in all neurons, trsn is transcriptionally upregulated in the heads of flies in response to starvation. Spatially restricted rescue or targeted knockdown localizes trsn function to neurons that produce the tachykinin family neuropeptide Leucokinin. Manipulation of neural activity in Leucokinin neurons revealed these neurons to be required for starvation-induced sleep suppression. Taken together, these findings establish trsn as an essential integrator of sleep and metabolic state, with implications for understanding the neural mechanism underlying sleep disruption in response to environmental perturbation.
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PMID:translin Is Required for Metabolic Regulation of Sleep. 2704 14


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