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)

In a flux chamber study of ion transport in human colon, we compared baseline rates with those measured during electrical stimulation of intrinsic nerves. In baseline studies, sodium was absorbed throughout, but maximally in transverse colon. In cecum, sodium absorption accounted for the short circuit current and chloride was not absorbed. Chloride was absorbed in transverse and sigmoid colon, however. Residual current was minimal in cecum and transverse colon, but increased in sigmoid colon. Neural stimulation caused chloride secretion in cecum, reduced chloride absorption in sigmoid colon, but caused no change in transverse colon; sodium absorption decreased in cecum. A neurotransmitter of unknown identity affects baseline short circuit current in sigmoid colon. Half of the increase in short circuit caused by neural stimulation in sigmoid colon is mediated by muscarinic receptors. The identity of the other transmitter(s) is not known. It is not substance P or histamine. The three divisions of the colon differ in relative rates of baseline ion transport and in their transport responses to intrinsic nerve stimulation.
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PMID:Ion transport in human cecum, transverse colon, and sigmoid colon in vitro. Baseline and response to electrical stimulation of intrinsic nerves. 243 53

Effective mucociliary clearance of secretions by airway mucosa requires efficient ciliary beating. The structure of airway secretions provides for this requirement by having a viscous mucous layer touched underneath and propelled by ciliary tips, while the rest of the cilium is surrounded by a serous fluid layer. The regulation of the latter layer is thought to be a function of mucosal epithelial cells capable of active ion transport. Mammalian medium-sized bronchi actively absorb sodium, whereas the tracheal mucosae of several mammals are capable of sodium absorption as well as chloride secretion. By generating local osmotic gradients, these ion transport processes may regulate the depth of the periciliary sol layer. These transport processes generate an electrical PD across the mucosa such that the luminal side is negatively charged in reference to the submucosal side (electrogenic transport). Transport of sodium and chloride across the plasma membrane is against a steep electrochemical gradient, and cellular energy resources are utilized for this purpose (active transport). Chloride transport is coupled to sodium transport; therefore, inhibition of the sodium pump (Na-K-ATPase) with ouabain leads to inhibition of sodium as well as chloride transport. Several neurohumoral agents have been found to stimulate chloride secretion, such as PGs, beta-adrenergic agonists, VIP, substance P, and bradykinin. Mechanisms of regulation of sodium transport by airway epithelia are not clearly understood. Available evidence suggests that elevation of cellular PGs, cAMP, and calcium enhances apical cell-membrane conductance to chloride ion, with an opposite effect on sodium conductance. Therefore, it seems reasonable to suggest that neurohumoral control mechanisms may switch from sodium and fluid absorption to chloride and fluid secretion, and vice versa. Several lines of evidence support this proposal. First, the lung of fetal lamb secretes chloride and fluid in utero; this activity ceases at birth, when the catecholamine level is increased, causing a decrease in chloride secretion. In contrast, adult sheep trachea absorbs sodium. Second, agents that stimulate chloride secretion in bovine trachea concomitantly reduce sodium absorption, and vice versa. Similar observations were noted in some instances in dog trachea. Third, whereas unstimulated ferret and cat tracheas only absorb sodium, they secrete chloride upon exposure to beta agonists.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Regulation of salt and water transport across airway mucosa. 287 93

The use of aerosolized furosemide has been increasing throughout Mexico, primarily because of its mechanism and site of action as well as its local and systemic effect. We hypothesize that its effect on the respiratory system is totally independent from its diuretic activity and that it is primarily caused by its interaction with the chlorine channels. Furthermore, there is also evidence that furosemide induces prostaglandin synthesis, blocks the sodium-calcium pump, producing relaxation of the smooth muscle that narrows the airway and causes reduced nerve responsiveness to the Neurokinin A produced in acute asthma attacks.
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PMID:Inhaled furosemide: a whole new mechanism of action. 1232 26

Inflammation is associated with various pulmonary diseases and contributes to the pathogenesis of acute lung injury. We previously identified a proinflammatory signaling pathway triggered by G protein-coupled receptors (GPCRs) in which stimulation of G(q)-coupled GPCRs results in activation of the transcription factor NF-kappaB. Because damage to the lung causes the release of multiple mediators acting through G(q)-coupled GPCRs, this signaling pathway is likely to contribute to inflammatory processes in the injured lung. In an effort to identify novel inhibitors of lung inflammation, the National Institutes of Health Clinical Collection, a library of 446 compounds, was screened for inhibitory activity toward production of IL-8 induced by stimulation of the G(q)-coupled tachykinin 1 receptor with substance P in A549 cells. Twenty-eight compounds that significantly inhibited substance P-induced IL-8 production were identified. The most potent inhibitor was triptolide, a diterpenoid compound from Tripterygium wilfordii Hook F, a vine used in traditional Chinese medicine for the treatment of autoimmune diseases. Triptolide inhibited IL-8 production induced by substance P with an IC(50) of 2.3 x 10(-8) M and inhibited NF-kappaB activation in response to an agonist of the protease-activated receptor 2 with an IC(50) of 1.4 x 10(-8) M. Anti-inflammatory effects of triptolide were assessed in vivo using a chlorine gas lung injury model in mice. Triptolide inhibited neutrophilic inflammation and the production of KC (Cxcl1) in the lungs of chlorine-exposed mice. The results demonstrate that triptolide exhibits anti-inflammatory activity in cultured lung cells and in an in vivo model of acute lung injury.
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PMID:Identification of triptolide, a natural diterpenoid compound, as an inhibitor of lung inflammation. 2034 78

Several cytoplasmic proteins that are involved in G protein-coupled receptor signaling cascades are known to translocate to the plasma membrane upon receptor activation, such as beta-arrestin2. Based on this example and in order to identify new cytoplasmic proteins implicated in the ON-and-OFF cycle of G protein-coupled receptor, a live-imaging screen of fluorescently labeled cytoplasmic proteins was performed using translocation criteria. The screening of 193 fluorescently tagged human proteins identified eight proteins that responded to activation of the tachykinin NK2 receptor by a change in their intracellular localization. Previously we have presented the functional characterization of one of these proteins, REDD1, that translocates to the plasma membrane. Here we report the results of the entire screening. The process of cell activation was recorded on videos at different time points and all the videos can be visualized on a dedicated website. The proteins BAIAP3 and BIN1, partially translocated to the plasma membrane upon activation of NK2 receptors. Proteins ARHGAP12 and PKM2 translocated toward membrane blebs. Three proteins that associate with the cytoskeleton were of particular interest : PLEKHH2 rearranged from individual dots located near the cell-substrate adhesion surface into lines of dots. The speriolin-like protein, SPATC1L, redistributed to cell-cell junctions. The Chloride intracellular Channel protein, CLIC2, translocated from actin-enriched plasma membrane bundles to cell-cell junctions upon activation of NK2 receptors. CLIC2, and one of its close paralogs, CLIC4, were further shown to respond with the same translocation pattern to muscarinic M3 and lysophosphatidic LPA receptors. This screen allowed us to identify potential actors in signaling pathways downstream of G protein-coupled receptors and could be scaled-up for high-content screening.
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PMID:A Fluorescent Live Imaging Screening Assay Based on Translocation Criteria Identifies Novel Cytoplasmic Proteins Implicated in G Protein-coupled Receptor Signaling Pathways. 2575 9

In this work it was carried out the bioremediation of water containing chlorides with native microalgae (MCA) provided by the Centre for study and research in biotechnology (CIBIOT) at Universidad Pontificia Bolivariana. Microalgae presented an adaptation to the water and so the conditions evaluated reaching a production of CO2 in mg L-1 of 53.0, 26.6, 56.0, 16.0 and 30.0 and chloride removal efficiencies of 16.37, 26.03, 40.04, 25.96 and 20.25% for microalgae1, microalgae2, microalgae3, microalgae4 and microalgae5 respectively. Water bioremediation process was carried out with content of chlorides in fed batch system with an initial concentration of chlorides of 20585 mg L-1 every 2 days. The Manipulated variables were: the flow of MCA3 (10% inoculum) for test one; NPK flow for test two, and flow of flow of MCA3+0.5 g L-1 NPK. Chloride removal efficiencies were 66.88%, 63.41% and 66.98% for test one, two and three respectively, for a total bioprocess time of 55 days.
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PMID:Potential of microalgae in the bioremediation of water with chloride content. 2906 64