Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

beta 1-Integrins are major mediators of interactions between cells and extracellular matrix (ECM). Adhesion of rat glomerular epithelial cells (GEC) to collagen stimulated phospholipase C. As a result, 1,2-diacylglycerol (DAG) was increased, and inositol phospholipids were decreased in collagen-adherent cells, as compared with GEC adherent to plastic substrata. Adhesion to collagen also stimulated production of free arachidonic acid (the precursor for eicosanoids) due to metabolism of DAG through the DAG lipase pathway and due to phospholipase A2-induced hydrolysis of phospholipids. Phospholipase A2 appeared to be stimulated as a result of protein kinase C (PKC) activation, probably secondary to increased DAG. The collagen-induced increases in DAG and free arachidonic acid, as well as the decrease in inositol phospholipids, were partially inhibited by lowering extracellular Ca2+ concentration to 200 nM or less and by anti-beta 1-integrin antibody Fab. In contrast, anti-beta 1-integrin immunoglobulin G (IgG) enhanced collagen-mediated increases in DAG and arachidonic acid. Proliferation of GEC adherent to collagen was reduced in the presence of anti-beta 1-integrin IgG. The antiproliferative effect of anti-beta 1-IgG appeared to be mediated through PKC, since it was absent in PKC-depleted GEC. Immunoprecipitation with integrin subunit-specific antibodies demonstrated alpha 2 beta 1- and alpha 3 beta 1-integrins in GEC. Thus, in GEC, ECM induces activation of phospholipases C and A2, which is mediated, at least in part, by beta 1-integrins. Products of integrin-mediated phospholipase activation may modulate GEC proliferation.
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PMID:Extracellular matrix-stimulated phospholipase activation is mediated by beta 1-integrin. 844 65

The majority of intra-abdominal adhesions develop postoperatively or following peritonitis. We have previously shown that L-phosphatidylcholine reduces postoperative peritoneal adhesions in rats. In the present study, we examined whether adhesion formation after bacterial peritonitis is also reduced by L-phosphatidylcholine or by DL-alpha-phosphatidylcholine, which is degraded only 50% by phospholipase A2. Peritonitis was induced in the rat by caecal ligation and double puncture; cecotomy was performed 12, 15, or 18 h later. Adhesions were assessed blindly by a scoring system 7 days after cecotomy. When cecotomy was scheduled for 18 h after caecal ligation and puncture, the 7-day mortality was 90% (n = 20). When cecotomy was performed at 12 h, no mortality was seen; however, the adhesion score was low (2.3 +/- 0.7). When cecotomy was performed 15 h after caecal ligation and puncture, the mortality was 25% and the adhesion score was 4.3 +/- 0.9. This figure was reduced significantly by intraperitoneal instillation of L-phosphatidylcholine or DL-alpha-phosphatidylcholine for 3 subsequent days. However, the mortality increased by L-phosphatidylcholine (P < 0.01), whereas mortality after DL-alpha-phosphatidylcholine remained at 30%. We conclude that administration of both L-phosphatidylcholine and DL-alpha-phosphatidylcholine decrease adhesion formation after bacterial peritonitis.
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PMID:Phospholipase-resistant phosphatidylcholine reduces intra-abdominal adhesions induced by bacterial peritonitis. 851 62

Adhesion formation is a major source of postoperative morbidity and mortality. Therefore, the reduction of postoperative adhesion formation would be of clinical benefit. Various modalities have been shown to reduce adhesion formation, including fibrinolytic enzymes, nonsteroidal anti-inflammatory drugs, and barriers that reduce the apposition of sites of potential adhesion formation. This study examined the ability of a phospholipase A2 inhibitor, anti-inflammatory peptide 2 (antinflammin), to reduce the formation of intraperitoneal adhesions in two rabbit models of adhesion formation. In the sidewall model, antinflammin was administered via Alzet miniosmotic pump for the entire postoperative interval, and there was a dose-dependent reduction in the area of the sidewall injury that was involved in adhesions to the cecum and the bowel. In the double uterine horn model, antinflammin was administered via Alzet miniosmotic pump to the area of injury for either 1, 2, 3, or 7 days. Administration of antinflammin for as little as 24 h after surgery significantly reduced the extent of adhesion formation. Administration of the peptide for longer periods of time did not further increase the reduction in adhesion formation. These studies clearly demonstrate that postoperative administration of antinflammin to the site of injury reduced the formation of postoperative adhesions in two animal models.
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PMID:Reduction of adhesion formation by intraperitoneal administration of anti-inflammatory peptide 2. 910 Jan 72

The cellular phospholipid, lysophosphatidic acid (LPA), released by activated platelets and fibroblasts or, at high levels, from ovarian and cervical carcinomas is a powerful serum mitogen that may modulate several signaling pathways in endothelial cells (EC). Hence, LPA could function in a paracrine manner during EC-platelet interactions at sites of vascular injury. Here, we demonstrate activation of the transcription factor nuclear factor kappa B (NF-kappaB) in EC following exposure to LPA. EC activation was further characterized by increased levels of mRNA transcripts encoding E-selectin, Intercellular Adhesion Molecule-1, Interleukin-8 and Monocyte Chemoattractant Protein-1. These effects were inhibited by preincubating EC either in the presence of mepacrine (to block phospholipase A2) or of pertussis toxin (to increase ADP-ribosylation of Gi proteins). No inhibition was observed in the presence of putative LPA receptor antagonists suramin or thrombospondin. LPA induces a proinflammatory activation of endothelial cells that (i) involves Gi proteins; (ii) depends on phospholipase A2 activity; (iii) is associated with the activation of NF-kappaB and (iv) results in increased expression of proinflammatory genes. We propose that LPA release by activated platelets may directly modulate vascular inflammatory responses.
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PMID:Lysophosphatidic acid activates nuclear factor kappa B and induces proinflammatory gene expression in endothelial cells. 1059 50

Adhesion and marginal permeability of materials used for fixation of whole-cast dentures and surface micro-relief were studied in vitro and in vivo on dogs. Three groups of materials were studied: zinc-phosphate, polycarboxylate, and glass-ionomeric. Polycarboxylate cements effectively fixed dentures irrespective of the status of abutment teeth, and glass-ionomeric cements w V.M. Marker and prognostic phospholipase A2 test in inflammatory diseases of the periodontium.
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PMID:[The fixation of nonremovable dentures: the rational choice of the material]. 1085 Jan 78

Adhesion to and internalization into host cells is an essential step in the pathogenesis of various bacterial infections. Here we investigated the effects of growth factors on the internalization of Escherichia coli O18 strains isolated from patients with urinary tract infection (UTI) by human epithelial cells. A dramatic increase in the uptake of Escherichia coli was observed after treatment of epithelial cells with epidermal growth factor (EGF) and to a lower extent with insulin. EGF-dependent internalization can be suppressed by tyrosine kinase inhibitors suggesting an involvement of the receptor tyrosine kinases in the regulation of the endocytotic process. Inhibitors of phospholipase A2, lipoxygenase, and cyclooxygenase significantly decreased internalization of bacteria induced by EGF. Finally, the specific inhibitor of PI 3-kinases Wortmannin was shown to suppress completely the EGF-independent internalization. The data of this analysis indicate the involvement of several signaling paths in bacterial internalization of uropathogenic Escherichia coli O18 strains and contribute to the comprehension of the pathogenesis of recurrent UTI.
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PMID:Internalization of extraintestinal Escherichia coli O18 strains by epithelial cells is modulated by EGF, insulin, and effectors of transmembrane signal transduction. 1104 83