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)

Adhesion proteins are cofactors in the aggregation of human platelets, and can mediate the ADP-induced response of these cells. It was shown that the synthetic cell adhesion peptide, Arg-Gly-Asp-Ser inhibits the aggregation of platelets from normal donors and ophthalmic patients with diabetic retinopathy, glaucoma and retinal vein occlusion. This effect increases in the relative order of activity retinal vein occlusion greater than or equal to glaucoma greater than or equal to diabetic retinopathy greater than control. Deaggregation due to the peptide appeared to be diminished in the order control (normal) greater than diabetic retinopathy greater than glaucoma greater than retinal vein occlusion after its addition at the maximum of aggregation curve. It is concluded that there are differences in the ability of Arg-Gly-Asp-Ser peptide to block the fibronectin adhesion receptor on ADP stimulated platelets from different clinical groups.
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PMID:Modulative effects of cell adhesion peptide (Arg-Gly-Asp-Ser) on the aggregation of stimulated platelets from ophthalmic patients. 182 18

Adhesion of the scleral flap is one of the postoperative complications in glaucoma surgery, especially in cases with trabeculectomy. From July 1989 to February 1990 a trabeculectomy was done in 102 patients with chronic open-angle glaucoma. To prevent adhesion of the scleral flap in the early postoperative period, a 9-0 nylon suture loop was fixed at the scleral flap and led through the conjunctiva. If in the early postoperative phase the intraocular pressure rose due to adhesion of the scleral flap, the flap was opened by pulling the suture loop and thereby releasing the scleral flap. The success of this method is indicated by the drop in intraocular pressure and the filling of the filtering bleb. In 31 of 102 patients an adhesion was observed. Twenty-four of these 31 patients recompensated after one or more pulls at the suture loop, causing the intraocular pressure to remain at a normal level.
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PMID:[Revision suture in covered goniotrepanation]. 812 16

The trabecular meshwork (TM), a specialized eye tissue, is a major site for regulation of the aqueous humor outflow. Malfunctioning of this tissue is believed to be responsible for development of glaucoma, a blinding disease. Myocilin is a gene linked to the most common form of glaucoma. The protein product has been localized to both intra and extracellular sites, but its function still remains unclear. This study was to determine whether extracellular myocilin presented in the matrix affects adhesion, morphology, and migratory and phagocytic activities of human TM cells in culture. Cell adhesion assays indicated that TM cells, while adhering readily on fibronectin, failed to attach on recombinant myocilin purified from bacterial cultures. Adhesion on fibronectin was also compromised by myocilin in a dose dependent manner. Myocilin in addition triggered TM cells to assume a stellate appearance with broad cell bodies and microspikes. Loss of actin stress fibers and focal adhesions was observed. TM cell migration on fibronectin/myocilin to scratched wounds was reduced compared to fibronectin controls. Myocilin, however, had little impact on phagocytic activities of TM cells. Cell attachment on fibronectin and migration of corneal fibroblasts, a control cell type, were not altered by myocilin. These results demonstrate that extracellular myocilin elicits anti-adhesive and counter-migratory effects on TM cells. Myocilin in the matrix of tissues could be exerting a similar influence on TM cells in vivo, impacting the flexibility and resilience required for maintenance of the normal aqueous outflow.
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PMID:Extracellular myocilin affects activity of human trabecular meshwork cells. 1513 56

Myocilin is a gene linked to the most common form of glaucoma, a major blinding disease. The trabecular meshwork (TM), a specialized eye tissue, is believed to be involved, at least in part, in the development of glaucoma. The myocilin expression is known to be up-regulated by glucocorticoids in TM cells, and an altered myocilin level may be the culprit in conditions such as corticosteroid glaucoma. Wild type myocilin, when transfected into cultured human TM cells, induced a dramatic loss of actin stress fibers and focal adhesions. Myocilin transfectants displayed a heightened sensitivity to trypsin. Adhesion to fibronectin, collagens, and vitronectin was compromised. The fibronectin deposition and the levels of fibronectin protein and mRNA were also reduced in myocilin transfectants. The fibronectin deposition could be restored by treatment with lysophosphatidic acid, a Rho stimulator. Assays further revealed that upon myocilin overexpression, the activity of RhoA was diminished, whereas the cAMP level and the protein kinase A (PKA) activity were augmented. Myocilin protein did not affect actin polymerization. The collapse of actin stress fibers and increased trypsin sensitivity from myocilin transfection could be reverted by co-expression of constitutively active RhoA or by treatment with PKA inhibitor H-89. The PKA activity, however, was not modified by co-expression of either constitutively active or dominant negative RhoA. These results demonstrate that myocilin has a de-adhesive activity and triggers signaling events. cAMP/PKA activation and the downstream Rho inhibition are possible mechanisms by which myocilin in overabundance may lead to TM cell or tissue damage.
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PMID:Rho GTPase and cAMP/protein kinase A signaling mediates myocilin-induced alterations in cultured human trabecular meshwork cells. 1798 96