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

To establish a selected salivary-gland cell culture and determine the effect of neuropeptides, monolayers were cultured using 3T3 cells as a feeder layer. To confirm the origin of these cultured cells, amylase production was examined by electron microscopy and periodic acid-Schiff staining, together with immunocytochemical analysis of myosin, anti-cytokeratin (CK-1, CK 10/13, CK MNF116, CK LMW, CK HMW and CK-19) and amylase antibody. The cultured cells demonstrated secretion granules containing amylase and presented features characteristic of acinar cells, which they retained until passage two. By using a feeder layer in conjunction with a newly formulated culture medium, the selectability of these cells was improved. Changes in proliferation of cultured salivary-gland cells in the presence of selected neurotransmitters were also examined. Isoproterenol enhanced cellular proliferation. On the other hand, vasoactive intestinal polypeptide and substance P, which increase the weight of salivary glands in vivo, showed no significant enhancement of proliferation.
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PMID:Selected salivary-gland cell culture and the effects of isoproterenol, vasoactive intestinal polypeptide and substance P. 873 10

The aims of this study were to detect the expression of intermediate filaments and to verify the existence of marker substances for neuronal and neuroendocrine cells within the interstitial Leydig cells of laboratory rodent's testes, such as it has been described in other species. Adult male rats, mice, gerbils, Syrian hamsters and guinea-pigs were used and the localization of the different markers was achieved by the streptoavidin-peroxidase immunohistochemical method. The present study demonstrates in all rodents studied a similar pattern of localization in Leydig cells of intermediate filaments (vimentin, cytokeratin, neurofilament 200 kD and glial fibrillary acidic protein) and other marker substances (S-100, CgA, substance P and neurone-specific enolase), which are typical of neuroendocrine (APUD cells or paraneurones) and glial cells. The expression of these substances, related to neurotransmitters or neurohomones and other proteins characteristic of neuroendocrine cells, could suggest that it is a neural crest derived cell. Although this study provides more evidences about the immunoexpression of neuronal and glial markers in Leydig cells, this fact cannot be related directly to their embryological origin, because the current data support the hypothesis of a mesenchymal origin of the Leydig cells.
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PMID:Immunohistochemical study of intermediate filaments and neuroendocrine marker expression in leydig cells of laboratory rodents. 1535 86

To test whether transient receptor potential channel vanilloid subfamily member-1 (TRPV1) mediates acid-induced inflammation in the esophagus, a tubular segment of esophageal mucosa was tied at both ends, forming a sac. The sac was filled with 0.01 N HCl (or Krebs buffer for control) and kept in oxygenated Krebs buffer at 37 degrees C. The medium around the sac (supernatant) was collected after 3 h. Supernatant of the HCl-filled sac abolished contraction of esophageal circular muscle strips in response to electric field stimulation. Contraction was similarly abolished by supernatant of mucosal sac filled with the TRPV1 agonist capsaicin (10(-6) M). These effects were reversed by the selective TRPV1 antagonist 5'-iodoresiniferatoxin (IRTX) and by the platelet-activating factor (PAF) receptor antagonist CV9388. Substance P and CGRP levels in mucosa and in supernatant increased in response to HCl, and these increases were abolished by IRTX and by tetrodotoxin (TTX) but not affected by CV9388, indicating that substance P and CGRP are neurally released and PAF independent. In contrast, the increase in PAF was blocked by IRTX but not by TTX. Presence of TRPV1 receptor was confirmed by RT-PCR and by Western blot analysis in whole mucosa and in esophageal epithelial cells enzymatically isolated and sorted by flow cytometry or immunoprecipitated with cytokeratin antibodies. In epithelial cells PAF increased in response to HCl, and the increase was abolished by IRTX. We conclude that HCl-induced activation of TRPV1 receptors in esophageal mucosa causes release of substance P and CGRP from neurons and release of PAF from epithelial cells.
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PMID:HCl-activated neural and epithelial vanilloid receptors (TRPV1) in cat esophageal mucosa. 1938 2

The ovulatory process is characterized by tissue wounding and, after oocyte expulsion, by healing being connected to the formation of a corpus luteum (CL). The ovulatory event thus compares with a sterile inflammation. The concept is forwarded that the ovulatory process depends on innate immunity (INIM) function. The ultimate trigger for INIM signaling are danger signals/alarmins from granulosa cells damaged by oxidative stress and reactive oxygen species (ROS), respectively. Alarmins like oxidized low density lipoprotein (oxLDL) are recognized by cytokeratin-positive (CK(+)) granulosa cells with the expression of toll-like receptor 4 (TLR4). The subsequent inside-out signaling from the antrum towards the thecal cell layer comprises inflammation and tissue disintegration, which might be dominated by the myeloid differentiation factor 88 (Myd88) gateway. Additive or co-regulatory function are expected from the complement cascade for vessel permeability and leukocyte immigration and the wingless (WnT)-signaling for cell adhesion of CK(+) granulosa cells. The outside-in signaling relates to the repair phase, which is primarily controlled by the TIR-domain-containing adaptor protein producing IFN type I (TRIF) gateway of TLR signaling. The KIT/CD117 tyrosine kinase receptor and the tachykinin-tachykinin receptor system could be involved. The appealing concept of INIM function in the ovary is novel and inaugurates a novel research field.
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PMID:Ovulation as danger signaling event of innate immunity. 2116 30


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