Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the first part of the study we analyzed the morphology of mast cells in autoimmune thyroiditis of BB/W rats. In the early stage of thyroiditis mast cells showed exocytosis of granules into the interstitium; this was associated with disorganization of the extracellular matrix and the appearance of a translucent ground substance in stroma. Mast cells were not seen in the mononuclear infiltrates in the later stages of thyroiditis. In order to further study the effect of mast cells on the extracellular matrix, we evaluated the effect of mast cell lysate and purified chymase on the matrix of cultured thyroid cells. Mast cells were obtained from peritoneal cavity; mast cell chymase was purified by anion exchange chromatography. After exposure to chymase there was a reduction of pericellular fibronectin in cultured thyroid cells, while laminin in matrix remained unchanged. Similarly, as found by gel electrophoresis, soluble fibronectin and vitronectin were digested by chymase in the reaction mixture. Cell attachment on both fibronectin and vitronectin was significantly decreased upon exposure of matrix proteins to chymase. The effects of chymase were abolished by enzyme inhibitor phenylmethane sulfonyl fluoride. These data suggest that mast cells possess proteolytic enzymes capable of digesting different host proteins which may have a role in the thyroid cell interaction with the surrounding matrix.
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PMID:The effect of mast cell chymase on extracellular matrix: studies in autoimmune thyroiditis and in cultured thyroid cells. 128 41

Chronic urticaria (CU) is a relatively common but vexing disease. The pathophysiology is based on the cutaneous mast cell release of mediators, predominantly histamine. Release can be induced via specific immunoglobulin E (IgE), components of complement activation and nonspecifically by various compounds including endogenous peptides, endorphins, and enkephalins. In >30% of CU patients, autoimmune phenomena have been found, characterized by positive autologous serum skin test, antibodies to the alpha-subunit of the basophil IgE receptor, to IgE itself, and, perhaps, the most clinically relevant, thyroid autoimmunity. Studies suggest that the products of the activated immune system can lower the cutaneous mast cell release threshold, possibly allowing activation by endogenous compounds. The resulting release of mediators produces the clinical picture of recurrent hives. Although the goal of management of CU is the identification of a treatable cause, in most CU patients, especially adults, a cause is not frequently found. Identified causes include drugs, foods, infections, immune complex production leading to urticarial vasculitis, autoantibody production, and underlying autoimmune disease, particularly autoimmune thyroiditis. The treatment of the thyroiditis with suppressive doses of thyroid hormone often results in the remission of the CU. Given the marginally effective and sometimes dangerous medical therapy available for CU, a systematic and thorough approach to identify a treatable cause in difficult CU patients is warranted.
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PMID:Chronic urticaria: pathophysiology and etiology, or the what and why. 1672 23