Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.1.1.148 (Thy1)
 1,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To assess the effects of high blood glucose concentration on glomerular changes after the acute mesangial cell injury in the rat, the monoclonal anti-Thy1.1 antibody OX-7 was injected into streptozoticin-induced diabetic rats or normal rats. The increase in proliferating cell nuclear antigen-positive cells in glomeruli at day 4 and glomerular hypercellularity at day 18 was less prominent in diabetic rats than in normal rats. The expansion of mesangial matrix area assessed by fibronectin immunostaining was more prominent, and segmental glomerulosclerosis was observed at day 60 in the diabetic rats. These data suggest that the insulin-deficient group may reflect impaired "wound-healing," leading to the prolonged ECM accumulation under the hyperglycemic condition in vivo.
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PMID:In vivo effects of hyperglycemia on the outcome of acute mesangial injury in rats. 782 41

Thymocyte development takes place in a complex milieu of supportive cells and ECM that are responsible for the proliferation, adhesion, migration, and selection processes these cells undergo before reaching maturity. In recent years, the role of notch signaling in lymphocyte development, specifically T-cell development, has been extensively characterized. Although notch ligand mediated signals have been shown to be a necessary component of T-cell generation from stem cells, high-throughput, synthetic biomaterial-based systems for notch-directed stem-cell differentiation into lymphocytes are yet to be reported. Here, we present a microbead-based, artificial notch signaling system to study stem-cell differentiation into the T-cell lineage. Magnetic microbeads were functionalized with the notch ligand DLL4 using streptavidin-biotin binding and antibody-antigen coupling. Immunohistochemistry and flow cytometry analysis indicated approximately 65% conjugation efficiency. Efficient notch signaling through these functionalized microbeads was demonstrated through a myotube inhibition assay in C2C12 myoblasts. Thy1.2(+) early T cells were successfully generated from mouse bone marrow hematopoietic stem cells (BMHSCs) using DLL4 functionalized beads using both insert-based and mixed stromal cell (OP9) coculture conditions, indicating that stem cell-stromal cell physical contact is not necessary for DLL4 directed T-cell differentiation. Coculture studies with bead-to-cell ratios of 1:1 generated higher T-cell differentiation efficiencies, compared to bead-to-cell ratios of 5:1. These data demonstrate the promising potential of this biomaterial-based notch signaling system to generate T cells from stem cells and to elucidate the molecular interactions in T-cell development.
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PMID:Biomaterial-based notch signaling for the differentiation of hematopoietic stem cells into T cells. 1684 70

We have previously identified the engulfment and cell motility 1 (ELMO1) as a susceptibility gene for diabetic nephropathy. To elucidate the role of ELMO1 in the pathogenesis of chronic renal injury, we examined the expression of Elmo1 in the kidney of a rat model for chronic glomerulonephritis (uninephrectomy plus anti-Thy1.1 antibody [E30] injection). We found that the expression of the Elmo1 was significantly increased in the renal cortex and glomeruli of uninephrectomized rats injected with E30 compared to controls. By in situ hybridization, the expression of Elmo1 was shown to be elevated in the diseased kidney, especially in glomerular epithelial cells. In COS cells, the overexpression of ELMO1 resulted in a substantial increase in fibronectin expression, whereas the depletion of the ELMO1 by small interfering RNA (siRNA) targeting ELMO1 significantly suppressed the fibronectin expression in ELMO1 overexpressing and control cells. We also found that the expression of integrin-linked kinase (ILK) was significantly increased in ELMO1 overexpressing cells, and the ELMO1-induced increase in fibronectin was partially, but significantly, inhibited by siRNA targeting ILK. Furthermore, we identified that the cell adhesion to ECMs was considerably inhibited in cells overexpressing ELMO1. These results suggest that the ELMO1 contributes to the development and progression of chronic glomerular injury through the dysregulation of ECM metabolism and the reduction in cell adhesive properties to ECMs.
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PMID:ELMO1 increases expression of extracellular matrix proteins and inhibits cell adhesion to ECMs. 1702