Disease relevance of Cell Degranulation

• Triggering of mast cells and basophils by immunoglobulin E (IgE) and antigen induces various biochemical signals, including tyrosine kinase activation, which lead to cell degranulation and the release of mediators of the allergic reaction [1].
• Surprisingly, intact DOCA-treated breeders also showed inhibition of arterial disease but they did have fatty livers and beta cell degranulation [2].
• It is suggested that tungstic acid effectively antagonizes stress-induced gastric ulcers, possibly by decreasing motility and mass cell degranulation [3].
• The toxic effect on the endocrine pancreas was manifest by hyperglycemia, glucosuria, islet atrophy and beta cell degranulation [4].

High impact information on Cell Degranulation

• Whereas 1-14 was found to increase PMA-induced cell degranulation significantly (175%), Ab 1-15 did not alter degranulation response to PMA [5].
• The intracellular granzyme B inhibitor, proteinase inhibitor 9, is up-regulated during accessory cell maturation and effector cell degranulation, and its overexpression enhances CTL potency [6].
• These results suggest that PI-9 serves to inactivate misdirected granzyme B following cytotoxic cell degranulation [7].
• This latter population is critical in maintaining Syk activity and cell degranulation [8].
• Inhibition of 5-lipoxygenase product formation and polymorphonuclear cell degranulation by tenidap sodium in patients with rheumatoid arthritis [9].

Biological context of Cell Degranulation

• Engagement of the high affinity IgE receptor (FcepsilonRI) with a multimeric antigen leads to immediate tyrosine phosphorylation of its beta and gamma subunits, recruitment, and activation of the tyrosine kinase Syk, and later to cell degranulation [8].
• Antigen stimulation of cultured bone-marrow-derived mast cells sensitized with specific monoclonal IgE induced cell degranulation and paf-acether (paf; 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine) biosynthesis via the deacylation/acetylation (remodelling) pathway [10].
• In contrast to IgE-mediated cell degranulation, expression of mRNA for c-fos was not dependent on continued receptor aggregation [11].
• The drug inhibits calcium-dependent events, such as interleukin-2 gene transcription, nitric oxide synthase activation, cell degranulation, and apoptosis [12].
• Cell death and stages of cell disruption including bleb cluster formation, loss of surface features, formation of membrane tears and holes, and cell degranulation correlated with Ni3S2 and TiO2 content [13].

Anatomical context of Cell Degranulation

• The supernatants enhance eosinophil helminthotoxicity by increasing cell degranulation; they also enhance the generation of leukotrienes in eosinophils by exerting a permissive effect on an early step of arachidonic acid metabolism [14].

Associations of Cell Degranulation with chemical compounds

• The PKC inhibitors chlorpromazine and staurosporine inhibited to a significant extent both cell degranulation and all steps leading to paf biosynthesis [10].
• CONCLUSION: Functional differences in metachromatic cell reactivity are present in atopic subjects 4h after in vivo allergen exposure which relate to the physiological response observed after this time and suggest that there is ongoing metachromatic cell degranulation subjects who subsequently develop LAR [15].
• Highly purified porcine phospholipase A2 induced noncytotoxic rat cell degranulation, as indicated by release of histamine without release of the cytoplasmic marker lactate dehydrogenase [16].
• Similar to IgE-mediated cell degranulation we demonstrated inhibition of the c-fos signal in the absence of calcium and after preincubation of cells with the protein tyrosine kinase inhibitor genistein [11].
• Similarly, MSH cell degranulation is more completely in 5-HTP-treated eels, which show simultaneously an unexplained dilatation of the swim-bladder not elicited by 5-HT treatment [17].

Gene context of Cell Degranulation

• These include a loss of GLUT2, glycogen accumulation, glucose recycling, abnormal glucokinase or hexokinase, altered mitochondrial glycerol phosphate dehydrogenase (mGPDH) activity, abnormal ion channel function and beta cell degranulation [18].
• These data suggest that the suppression of cortisol synthesis is responsible for the stimulation of the CRF ir-perikarya and the CRF release along the rostral pars distalis, inducing ACTH cell degranulation [19].
• Activation of RBL-2H3 cells by short term PMA treatment failed to induce cell degranulation or expression of mRNA for c-fos [11].
• Anti-OVA antisera with PCA titers of 1/32 to 1/64 failed to stimulate RBL cell degranulation, whereas high titer antibody (1/2048 to 1/4096 by PCA) induced a positive RBL cell response [20].

References