Modification of LTBP-1S 53 gene in HGEC may abrogate fibrotic action of TGF- 1 but this requires confirmation. Major splice variant of LTBP-1 in HGEC was LTBP-1S 53. In conclusion, HGEC express LTBP-1 mRNA which is suppressed at basal state but upregulated by high glucose, H2O2, and TGF- 1 and downregulated by VEGF. TGF- 1, but not high glucose, H2O2 or VEGF, tended to increase LTBP-1S 53 mRNA. Of 12 clones selected randomly, Sca I mapping and DNA sequencing revealed that only one was LTBP-1S and all the others were LTBP-1S 53. RT-PCR with a primer set for LTBP-1S produced many clones but no clone was gained with a primer set for LTBP-1L. High glucose, H2O2, and TGF- 1 upregulated and vascular endothelial growth factor (VEGF) further downregulated LTBP-1 mRNA in HGEC. Basal expression of LTBP-1 mRNA was suppressed in HGEC compared to WI-38 human embryonic lung fibroblasts. To elucidate the cell specific expression of the genes of LTBP-1 and their splice variants and the factors that regulate the gene expression, we cultured primary human glomerular endothelial cells (HGEC) under different conditions. PMID 8717512.Latent transforming growth factor (TGF)-binding protein (LTBP) is required for the assembly, secretion, matrix association, and activation of latent TGF- complex. "The interleukin-2 receptor gamma chain: its role in the multiple cytokine receptor complexes and T cell development in XSCID". "Interleukin-12 dependent interferon-g production by CD8a + lymphoid dendritic cells". "Modulation of hematopoiesis in mice with a truncated mutant of the interleukin-2 receptor gamma chain". "Lymphohaematopoietic abnormalities and systemic lymphoproliferative disorder in interleukin-2 receptor gamma chain-deficient mice".
"DNA-dependent kinase (p350) as a candidate gene for the murine SCID defect". "A severe combined immunodeficiency mutation in the mouse". The formal names for the NOD-scid IL2rgnull mice are NOD.Cg-PrkdcscidIl2rgtm1Sug. Our experimental studies with human hematopoietic stem cells transferred to NOG mice demonstrated that they were extremely efficient for humanized mice. "Breeding of a non-obese, diabetic strain of mice". group in 1996 on NOD/Shi-scid mice by a 10th generation backcross mating in 2000. White1, and Sebastien Monette1 Abstract In the past decade, NOD. The murine autoimmune diabetes model: NOD and related strains. Laboratory AnimalsOriginal Article Pathology of Aging in NOD scid gamma Female Mice Sara F. "Multiple defects in innate and adaptive immunologic function in NOD/LtSz-scid mice". "NOD/SCID/γ null mouse: an excellent recipient mouse model for engraftment of human cells". Lack of NK cells, dendritic cell dysfunctions, and other unknown deficiencies due to inactivation of the IL-2Rγ gene.Lack of functional T and B cells that is derived from a mutation of protein kinase (Prkdc: protein kinase, DNA activated, catalytic polypeptide), which is the causative gene of the scid mutation.as autoimmune non-obese-type diabetes mice. The NOD/Shi inbred strain was first discovered by Makino et al. Reduced innate immunity derived from a NOD inbred strain, which involves a macrophage dysfunction, and a defect of complement hemolytic activity and reduced NK activity.NOG mouse has multiple immunodeficiencies that are principally derived from three strains of mice: 1) NOD/Shi inbred strain, 2) SCID, 3) IL-2Rγ null. No leakiness: no incidence of T, B cells with aging.Although this approach successfully provides human immune microenvironment in recipients, it necessitates the procurement of human fetal tissues. NOD/SCID mice have been used as a model of this type in. No activity of T cell, B cell and NK cell NOD/SCID/BLT system supports functional human T-cell development by meeting this requirement through implantation of fetal thymic and liver tissues into NOD/SCID mice. Natural killer (NK) cell-deficient mice are useful models in biomedical research.The NOG mouse was generated in CIEA in 2000 by back-cross mating of C57BL/6J-IL-2Rγ null mouse that was originally developed by Kazuo Sugamura, a professor of Tohoku University, to NOD/Shi- scid mouse that was developed in CIEA.
0 kommentar(er)
