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

The high iron diamine (HID) method has been found to impart density at the ultrastructural level selectively to sites known to contain sulphated complex carbohydrates. Thus, immature primary granules in rabbit heterophils, immature precrystalloid granules in rabbit eosinophils, all granules of rabbit basophils, mouse and rat mast cells and the nucleoids of alpha-granules of rabbit platelets were stained by HID. Granules of mast cells in rat cervical lymph node varied in the distribution pattern of the HID-reactive component. Mucous droplets within goblets of mouse colonic epithelial cells varied in HID reactivity. Sites known to contain sialomucin but no sulphates, such as mucous cells and apical plasmalemmae in mouse rectosigmoid colon, failed to stain with HID in contrast to their reactivity of dialysed iron at the ultrastructural level. The surface of mast cells and blood cells lacked affinity for HID, indicating that the dialysed iron binding at the surfaces can be attributed to neuraminic acid. HID proved more effective than dialysed iron in visualizing acid mucosubstance in precursor forms of the crystalloid granules in the eosinophil and in mast cell granules. Inclusion of 0.5% glycerol in the HID solution enhanced staining in mouse colon.
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PMID:Ultrastructural visualization of sulphated complex carbohydrates in blood and epithelial cells with the high iron diamine procedure. 7 22

CD34 is a cell-surface sialomucin expressed by hematopoietic stem cells (HSC), mast cells, and vascular endothelia. Despite its popularity as an HSC marker, the function of CD34 on hematopoietic cells remains enigmatic. Here, we have addressed this issue by examining the behavior of mutant mast cells lacking CD34, the related sialomucin, CD43, or both molecules. Loss of these molecules leads to a gene-dose-dependent increase in mast cell homotypic aggregation with CD34/CD43KOs > CD43KO > CD34KO > wild-type. Importantly, reexpression of CD34 or CD43 in these cells caused reversal of this phenotype. Furthermore, we find that loss of these sialomucins prevents mast cell repopulation and hematopoietic precursor reconstitution in vivo. Our data provide clear-cut evidence for a hematopoietic function for CD34 and suggest that it acts as a negative regulator of cell adhesion.
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PMID:CD34 and CD43 inhibit mast cell adhesion and are required for optimal mast cell reconstitution. 1566 58

Asthma is a pulmonary inflammatory disease dependent on eosinophil and mast cell infiltration into the lung. CD34 is a sialomucin expressed by both of these cell types, and we have used CD34(-/-) mice and a standard mouse model of asthma to evaluate the importance of CD34 expression on disease development. In comparison with wild-type (wt) mice, CD34(-/-) mice exhibited a dramatic reduction in all hallmarks of allergic asthma, including lowered airway inflammatory cell infiltration, airway hyperresponsiveness, and mast-cell recruitment. Bone marrow transplantation experiments confirmed that these defects are due to CD34 expression by bone marrow-derived cells. This was not, however, due to an inability to respond to antigen as, on a per cell basis, wt and CD34(-/-) inflammatory cells exhibit identical responses in cytokine production. We found a striking reduction in mobility of CD34(-/-) eosinophils in vitro, the major component of inflammatory infiltrates, which was consistent with proposed models for CD34 as an inhibitor of cell-cell adhesion. In summary, our data suggest that CD34 enhances mast-cell and eosinophil invasiveness and that its expression by these cells is a prerequisite for development of allergic asthma.
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PMID:CD34 facilitates the development of allergic asthma. 1755 98

CD34 is a cell surface sialomucin expressed by hematopoietic precursors, eosinophils, mast cells, and vascular endothelia and is suggested to play an integral role in mucosal inflammatory responses. Although Cd34(-/-) mice have normal hematopoietic cell subsets in peripheral tissues at steady state, they exhibit a cell recruitment defect when challenged, offering a unique opportunity to distinguish between local inflammatory cell proliferation and peripheral recruitment in disease. Autoimmune arthritis is an inflammatory disease dependent on hematopoietic infiltration, and in this study, we have examined the role of CD34 in disease development and progression. Using an autoimmune serum transfer model, arthritis was induced in C57BL/6 wild-type and Cd34(-/-) mice. Surprisingly, we found that Cd34(-/-) mice were more susceptible to arthritis than wild-type mice. We examined mast cell-transplanted, eosinophil-deficient, and bone marrow-chimeric mice to determine the role of CD34 expression on disease progression. These experiments excluded CD34-deficient mast cells, eosinophils, or hematopoietic cells as the cause of the exacerbated disease. Further study demonstrated that Cd34(-/-) mice exhibit increased vascular leakage at onset of disease and in response to TNF, which correlated with a subsequent increase in disease severity. We conclude that loss of CD34 expression leads to increased vascular permeability in the joints at onset of disease, leading to exacerbated arthritic disease in Cd34(-/-) mice.
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PMID:Loss of CD34 leads to exacerbated autoimmune arthritis through increased vascular permeability. 2003 36

Airway hyperresponsiveness (AHR), a major hallmark of asthma, results from alterations of contractile and noncontractile elements of airway reactivity. CD34 is a sialomucin that is expressed on various cells involved in asthma, such as eosinophils and airway smooth muscle precursors, highlighting its potential influence in AHR. To study the role of CD34 in regulating the contractile and noncontractile elements of AHR, AHR was induced by chronic exposure to house dust mite (HDM) antigen. To assess the role of CD34 on the contractile elements of AHR, airway reactivity and airway smooth muscle contractility in response to methacholine were measured. To assess CD34's role in regulating the noncontractile elements of AHR, a chimeric mouse model was used to determine the impact of CD34 expression on inflammatory versus microenvironmental cells in AHR development. Extracellular matrix production, mucus production, and mast cell degranulation were also measured. Whereas wild-type mice developed AHR in response to HDM, a loss of airway reactivity was observed in Cd34-/- mice 24 hours after the last exposure to HDM compared with naive controls. This was reversed when airway reactivity was measured 1 week after the last HDM exposure. Additionally, mast cell degranulation and mucus production were altered in the absence of CD34 expression. Importantly, simultaneous expression of CD34 on cells originating from the hematopoietic compartment and the microenvironment was needed for expression of this phenotype. These results provide evidence that CD34 is required for AHR and airway reactivity maintenance in the early days after an inflammatory episode in asthma.
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PMID:CD34 Differentially Regulates Contractile and Noncontractile Elements of Airway Reactivity. 2885 Feb 57