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Chemical Compound Review

AG-K-10159     1,8-dimethyl-5-phenyl- phenazine-2,7...

Synonyms: SureCN1502460, AC1L1UMB, CTK5D9369, AR-1D5177, AKOS015916442, ...
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Disease relevance of 1,8-dimethyl-5-phenyl-phenazine-2,7-diamine

  • Isolated kidney proximal tubules subjected to hypoxia/reoxygenation (H/R) have incomplete recovery of mitochondrial membrane potential (DeltaPsi(m)) that can be improved, but not normalized, by ATP in permeabilized cells as measured by safranin O uptake [1].
  • Evaluation of a safranin-O-stained antigen microagglutination test for francisella tularensis antibodies [2].
  • If the tibial cartilage is separated from the bony collar and cultured alone in serum-free medium, the nonhypertrophic chondrocytes also hypertrophy; the matrix loses Safranin O staining; however, some components of the matrix including type X collagen still remain after 30 days [3].
  • Safranin O-stained antigen microagglutination test for detection of brucella antibodies [4].
  • A microagglutination test with safranin-stained Francisella tularensis antigen was compared with a conventional tube agglutination test for the serodiagnosis of tularemia [5].
 

High impact information on 1,8-dimethyl-5-phenyl-phenazine-2,7-diamine

  • Although rKL-developed BMMC were safranin+ and produced substantial amounts of 35S-labeled heparin proteoglycans, they contained only minimal amounts of histamine and MC-CPA enzymatic activity relative to serosal MC [6].
  • Mast cells also developed on the glandular stomach mucosa, but these cells stained with alcian blue rather than safranin, and did not stain with berberine sulfate [7].
  • Similar bottlebrush structures were observed in the intercellular matrix of the smooth muscle cell cultures after staining with Safranin 0 [8].
  • We have evaluated this hypothesis by examining the immunofluorescent localization and concentrations of proteoglycan monomer core protein and link protein, and the concentrations of glycosaminoglycans demonstrated by safranin 0 staining, in the different zones of the bovine fetal cartilage growth plate [9].
  • Safranin O staining demonstrated that articular cartilage was well preserved in IL-6 -/- mice, whereas it was destroyed completely in IL-6 +/+ mice [10].
 

Chemical compound and disease context of 1,8-dimethyl-5-phenyl-phenazine-2,7-diamine

 

Biological context of 1,8-dimethyl-5-phenyl-phenazine-2,7-diamine

  • Wild-type peritoneal mast cells had a mature phenotype characterized by differential histochemical staining with proteoglycan-reactive dyes (cells do not stain with alcian blue but stain with safranin and with berberine) and a high side scatter to forward scatter ratio by flow cytometry and were detergent resistant [16].
  • Absorbance shifts in safranine have been used as a probe to estimate the membrane potential generated under these conditions [17].
  • Histology and immunohistochemistry revealed a dramatic decrease in Safranin O staining and reduced anti-aggrecan staining (primarily in the superficial and middle cartilage layers) with OP-1 antisense treatment [18].
  • Electron microscopy was applied to demonstrate morphologic changes, and Safranin O staining was performed to analyze the relationship between apoptosis and proteoglycan depletion [19].
  • Three weeks after injection, cell death and loss of Safranin O staining had progressed, and surface fibrillation and osteophytes had developed [20].
 

Anatomical context of 1,8-dimethyl-5-phenyl-phenazine-2,7-diamine

  • After 12-14 days of coculture, greater than 50% of the BMMC changed histochemically to become safranin+; 30-40% of the 35S-labeled glycosaminoglycans on the proteoglycans synthesized by these cocultured mast cells were heparin, whereas heparin was not detected in the initial BMMC [21].
  • Secretory granules of the rat basophilic leukemia (RBL-1) cell, a chemically generated tumor cell line maintained in tissue culture, were shown to stain with alcian blue but not with safranin counterstain and to have sparse, small, electron-dense granules [22].
  • A phenotypic change from safranin-negative to safranin-positive cells associated with heparin-producing CTMCs was accomplished after coculture of the mast cells with fibroblast cell lines derived from normal mice or from SI/SId mice plus soluble factors [23].
  • Furthermore, expression of these receptors restored the capacity of W/Wv BMMCs to colonize the peritoneal cavity of mast cell-deficient W/Wv mice where they differentiated to safranin-positive cells with similar frequencies as wild-type BMMCs [24].
  • The alcian-blue-safranin technique delineated the maturation of mast cell granules by showing the loss of alcian-blue and increase in safranin-positive organelles presumed to reflect the increase in N-sulfated polysaccharides representing heparin [25].
 

Associations of 1,8-dimethyl-5-phenyl-phenazine-2,7-diamine with other chemical compounds

 

Gene context of 1,8-dimethyl-5-phenyl-phenazine-2,7-diamine

  • In culture, all three receptor molecules transduced functional mitogenic signals in infected interleukin-3 (IL-3)-dependent bone marrow-derived mast cells (BMMCs) and enabled their differentiation into safranin-positive mast cells resembling connective tissue-type mast cells (CTMCs) [24].
  • Hyaluronan accumulation was characterized by staining with a hyaluronan-specific binding protein and by fluorophore-assisted carbohydrate electrophoresis, while proteoglycan content was determined by alcian blue and Safranin O staining, CD44 protein expression by immunohistochemistry, and aggrecan biosynthesis by 35S-sulfate incorporation [30].
  • However, Safranin O-stained sections from the Jnk2(-/-) mice exhibited significantly less joint damage [31].
  • Treatment of normal articular cartilage with RANTES increased the release of glycosaminoglycans and profoundly reduced the intensity of Safranin O staining [32].
  • The loss of aggrecan in Safranin O-stained sections was quantified by morphometric methods [33].
 

Analytical, diagnostic and therapeutic context of 1,8-dimethyl-5-phenyl-phenazine-2,7-diamine

  • At 24 hr after hepatectomy, absorbance change of safranine O per milligram of mitochondrial protein increased from 15.0 +/- 2.2 X 10(-3) to 37.4 +/- 3.3 X 10(-3) per mg (p less than 0.005) [34].
  • Cartilage damage and activation of BMP signaling were studied by digital image analysis using Safranin O sulfated glycosaminoglycan staining and immunohistochemistry for phosphorylated Smads (Smads 1, 5, and 8), respectively [35].
  • End-point analyses included macroscopic joint examination, immuno- and TUNEL staining, Safranin O staining/microspectrophotometry, and tumor necrosis factor alpha (TNFalpha) convertase enzyme (TACE) inhibition assay [36].
  • In striking contrast, when triamcinolone hexacetonide was injected into the ipsilateral knee 24 hours after the intraarticular injection of iodoacetate, fibrillation was noted in only 1 of 6 samples, osteophytes were much less prominent, pericellular staining with Safranin O persisted, and cell loss was less extensive [37].
  • The preferential binding of NADP+ to reduced enzyme permits prediction of a more positive oxidation-reduction potential of the flavoprotein in the presence of NADP+; a change of about + 0.1 V has been demonstrated by titration with safranine T [38].

References

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  2. Evaluation of a safranin-O-stained antigen microagglutination test for francisella tularensis antibodies. Brown, S.L., McKinney, F.T., Klein, G.C., Jones, W.L. J. Clin. Microbiol. (1980) [Pubmed]
  3. The influence of bone and marrow on cartilage hypertrophy and degradation during 30-day serum-free culture of the embryonic chick tibia. Cole, A.A., Luchene, L.J., Linsenmayer, T.F., Schmid, T.M. Dev. Dyn. (1992) [Pubmed]
  4. Safranin O-stained antigen microagglutination test for detection of brucella antibodies. Brown, S.L., Klein, G.C., McKinney, F.T., Jones, W.L. J. Clin. Microbiol. (1981) [Pubmed]
  5. Microagglutination test for early and specific serodiagnosis of tularemia. Sato, T., Fujita, H., Ohara, Y., Homma, M. J. Clin. Microbiol. (1990) [Pubmed]
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  18. Antisense inhibition of osteogenic protein 1 disturbs human articular cartilage integrity. Söder, S., Hakimiyan, A., Rueger, D.C., Kuettner, K.E., Aigner, T., Chubinskaya, S. Arthritis Rheum. (2005) [Pubmed]
  19. Linkage of chondrocyte apoptosis and cartilage degradation in human osteoarthritis. Hashimoto, S., Ochs, R.L., Komiya, S., Lotz, M. Arthritis Rheum. (1998) [Pubmed]
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  22. Homology of the rat basophilic leukemia cell and the rat mucosal mast cell. Seldin, D.C., Adelman, S., Austen, K.F., Stevens, R.L., Hein, A., Caulfield, J.P., Woodbury, R.G. Proc. Natl. Acad. Sci. U.S.A. (1985) [Pubmed]
  23. Cofactors are essential for stem cell factor-dependent growth and maturation of mast cell progenitors: comparative effects of interleukin-3 (IL-3), IL-4, IL-10, and fibroblasts. Rennick, D., Hunte, B., Holland, G., Thompson-Snipes, L. Blood (1995) [Pubmed]
  24. Rescue of W-associated mast cell defects in W/Wv bone marrow cells by ectopic expression of normal and mutant epidermal growth factor receptors. von Rüden, T., Stingl, L., Ullrich, A., Wagner, E.F. Blood (1993) [Pubmed]
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  26. Reduction of arthritis severity in protease-activated receptor-deficient mice. Yang, Y.H., Hall, P., Little, C.B., Fosang, A.J., Milenkovski, G., Santos, L., Xue, J., Tipping, P., Morand, E.F. Arthritis Rheum. (2005) [Pubmed]
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  30. Stimulation of hyaluronan metabolism by interleukin-1alpha in human articular cartilage. Nishida, Y., D'Souza, A.L., Thonar, E.J., Knudson, W. Arthritis Rheum. (2000) [Pubmed]
  31. Joint damage and inflammation in c-Jun N-terminal kinase 2 knockout mice with passive murine collagen-induced arthritis. Han, Z., Chang, L., Yamanishi, Y., Karin, M., Firestein, G.S. Arthritis Rheum. (2002) [Pubmed]
  32. Production of the chemokine RANTES by articular chondrocytes and role in cartilage degradation. Alaaeddine, N., Olee, T., Hashimoto, S., Creighton-Achermann, L., Lotz, M. Arthritis Rheum. (2001) [Pubmed]
  33. Cartilage-specific constitutive expression of TSG-6 protein (product of tumor necrosis factor alpha-stimulated gene 6) provides a chondroprotective, but not antiinflammatory, effect in antigen-induced arthritis. Glant, T.T., Kamath, R.V., Bárdos, T., Gál, I., Szántó, S., Murad, Y.M., Sandy, J.D., Mort, J.S., Roughley, P.J., Mikecz, K. Arthritis Rheum. (2002) [Pubmed]
  34. Biological significance of enhanced mitochondrial membrane potential in regenerating liver. Nishihira, T., Tanaka, J., Nishikawa, K., Jikko, A., Taki, Y., Morimoto, T., Koizumi, K., Kamiyama, Y., Ozawa, K., Tobe, T. Hepatology (1986) [Pubmed]
  35. Noggin haploinsufficiency differentially affects tissue responses in destructive and remodeling arthritis. Lories, R.J., Daans, M., Derese, I., Matthys, P., Kasran, A., Tylzanowski, P., Ceuppens, J.L., Luyten, F.P. Arthritis Rheum. (2006) [Pubmed]
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