Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.4.37 (CNPase)
 539 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this paper, the characterization of four human malignant glioma cell lines is described. The four lines are positive for glial fibrillary acidic protein (GFAP) in variable amounts. One of them, LN 992, is positive for S-100 protein. Myelin basic protein could not be detected in any of the four lines. The four lines had high levels of CNPase activity. The karyotype shows polyploidy for all lines, with modal numbers ranging from 80 to 120 and various numbers of marker chromosomes. Particular attention has been paid to the surface phenotype and a panel of three antiglioma monoclonal antibodies (Mabs), five antimelanoma Mabs, one anti-CALLA Mab, and two anti-HLA-DR Mabs has been used in an antibody-binding radioimmunoassay for the four cell lines. Lines LN 215 and LN 235 are positive with two antiglioma Mabs, LN 992 is negative. The four lines are positive with all five antimelanoma Mabs, except for LN 992 which ist negative with Mab D5. LN 992 and LN 215 are positive with the anti-CALLA Mab N2A12. LN 308 and LN 992 are positive with anti-HLA-DR Mab D4-22. There was no correlation between the in vitro morphology of the lines and the expression of the various biochemical or surface markers. These results stress the heterogeneity of the phenotype of human malignant glioma lines. These lines will be useful tools for further immunologic studies.
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PMID:Characterization of four human malignant glioma cell lines. 299 Jan 47

Diffuse traumatic brain injury (TBI) initiates secondary pathology, including inflammation and reduced myelination. Considering these injury-related pathologies, the many states of activated microglia as demonstrated by differing morphologies would form, migrate, and function in and through fields of growth-inhibitory myelin byproduct, specifically Nogo. Here we evaluate the relationship between inflammation and reduced myelin antigenicity in the wake of diffuse TBI and present the hypothesis that the Nogo-66 receptor antagonist peptide NEP(1-40) would reverse the injury-induced shift in distribution of microglia morphologies by limiting myelin-based inhibition. Adult male rats were subjected to midline fluid percussion sham or brain injury. At 2h, 6h, 1d, 2d, 7d, and 21d post-injury, immunohistochemical staining was analyzed in sensory cortex (S1BF) for myelin antigens (myelin basic protein; MBP and CNPase), microglia morphology (ionized calcium-binding adapter protein; Iba1), Nogo receptor and Nogo. Pronounced reduction in myelin antigenicity was evident transiently at 1d post-injury, as evidenced by decreased MBP and CNPase staining, as well as loss of white matter organization, compared to sham and later injury time points. Concomitant with reduced myelin antigenicity, injury shifted microglia morphology from the predominantly ramified morphology observed in sham-injured cortex to hyper-ramified, activated, fully activated, or rod. Changes in microglial morphology were evident as early as 2h post-injury, and remained at least until day 21. Additional cohorts of uninjured and brain-injured animals received vehicle or drug (NEP(1-40), i.p., 15min and 19h post-injury) and brains were collected at 2h, 6h, 1d, 2d, or 7d post-injury. NEP(1-40) administration further shifted distributions of microglia away from an injury-induced activated morphology toward greater proportions of rod and macrophage-like morphologies compared to vehicle-treated. By 7d post-injury, no differences in the distributions of microglia were noted between vehicle and NEP(1-40). This study begins to link secondary pathologies of white matter damage and inflammation after diffuse TBI. In the injured brain, secondary pathologies co-occur and likely interact, with consequences for neuronal circuit disruption leading to neurological symptoms.
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PMID:Nogo presence is inversely associated with shifts in cortical microglial morphology following experimental diffuse brain injury. 2873 37