Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.7.6 (RNA polymerase)
 34,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the effects of Icariin on expression of osteopontin (OPN) mRNA and type I collagen in rat osteoblasts in vitro and to explore its possible mechanisms in preventing osteoporosis. OB was isolated from calvaria of new-born new-born fetal Sprague-Dawley (SD) rats by means of modified sequential collagenase digestion and incubated in MEM medium and the cell morphology was observed under inverted phase contrast microscope, OB was identified by alkaline phosphatase (ALP) staining. Different concentration (0.1 microg/mL, 1.0 microg/ml, 10 microg/mL) of Icariin was added to the OB and incubated. The effect of Icariin on the proliferation and osteogenesis of OB was monitored by MTT analysis. The expression of type I collagen was estimated with immunohistochemistry techniques. The expression levels of mRNA of OPN in the cells in every group were examined by reverse-transcriptase ploymerase chain reaction (RT-PCR). The expression of OPN mRNA and type I collagen was strengthened gradually with the increase of Icariin concentration and peaked with 10 microg/mL Icariin on the 5th day. Icariin could significantly promote the expression of OPN mRNA and type I collagen in rat osteoblasts in vitro. The levels of expression of OPN mRNA and type I collagen were changed with different concentration of Icariin. Icariin could effectively prevent and treat osteoporosis and promote the bone formation.
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PMID:Effects of Icariin on expression of OPN mRNA and type I collagen in rat osteoblasts in vitro. 1669 27

The surface properties of a biomaterial are fundamental to determine the response of the host tissue. In the present study, we have followed a particular biomimetic strategy where electromagnetically stimulated SAOS-2 human osteoblasts proliferated and built a calcified extracellular matrix on a titanium fiber-mesh surface. In comparison with control conditions, the electromagnetic stimulation (magnetic field intensity, 2 mT; frequency, 75 Hz) caused higher cell proliferation and increased surface coating with type-I collagen, decorin, and osteopontin (9.8-fold, 11.3-fold, and 9.5-fold, respectively). Reverse transcriptase-polymerase analysis revealed the electromagnetically upregulated transcription specific for the foregoing matrix proteins and for the growth factor TGF-beta1. The immunofluorescence of type-I collagen, decorin, and osteopontin showed their colocalization in the cell-rich areas. The use of an electromagnetic bioreactor aimed at obtaining the surface modification of the biocompatible metallic scaffold in terms of cell colonization and coating with calcified extracellular matrix. The superficially modified biomaterial could be used, in clinical applications, as an implant for bone repair.
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PMID:Electromagnetic enhancement of a culture of human SAOS-2 osteoblasts seeded onto titanium fiber-mesh scaffolds. 1820 May 42

Runx2 is a member of the Runx family of transcription factors (Runx1-3) with a restricted expression pattern. It has so far been detected predominantly in skeletal tissues where, inter alia, it regulates the expression of the beta-galactoside-specific lectin galectin-3. Here we show that, in contrast to Runx3, Runx1 and Runx2 are expressed in a variety of human glioma cells. Runx2 expression pattern in these cells correlated completely with that of galectin-3, but not with that of other galectins. A similar correlation in the expression pattern of galectin-3 and Runx2 transcripts was detected in distinct types of 70 primary neural tumors, such as glioblastoma multiforme, but not in others, such as gangliocytomas. In glioma cells, Runx2 is directly involved in the regulation of galectin-3 expression, as shown by RNAi and transcription factor binding assays demonstrating that Runx2 interacts with a Runx2-binding motif present in the human galectin-3 promoter. Knockdown of Runx2 was thus accompanied by a reduction of both galectin-3 mRNA and protein levels by at least 50%, dependent on the glial tumor cell line tested. Reverse transcriptase-polymerase chain reaction analyses, aimed at finding other potential target genes of Runx2 in glial tumor cells, revealed the presence of bone sialoprotein, osteocalcin, osteopontin, and osteoprotegerin. However, their expression patterns only partially overlap with that of Runx2. These data suggest a functional contribution of Runx-2-regulated galectin-3 expression to glial tumor malignancy.
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PMID:Runx2 is expressed in human glioma cells and mediates the expression of galectin-3. 1843 28

Mesenchymal stem cells (MSCs) are self-renewing cells that exhibit differentiation capacity and immune regulation ability. These versatile cells have a wide range of potential applications. However, the spontaneous differentiation and aging of MSCs during long-term culturing restrict the amount of cells available for therapies and tissue engineering. Thus, maintaining the biological characteristics of MSCs during long-term culturing is crucial. Chromatic modification via epigenetic regulatory mechanisms (e.g., histone acetylation, deacetylation, and methylation) is crucial in stem cell pluripotency. We investigated the effects of largazole or trichostatin A (TSA), a novel histone deacetylase inhibitor (HDACi), against human umbilical cord (hUC)-MSCs aging. Results show that low concentrations of largazole or TSA can significantly improve hUC-MSCs proliferation and delay hUC-MSCs aging. Largazole can better improve MSCs proliferation than TSA. HDAC is modulate histone H3 acetylation and methylation in the telomerase reverse-transcriptase, octamer-binding transcription factor 4, Nanog, C-X-C chemokine receptor 4, alkaline phosphatase, and osteopontin genes. HDACis can promote hUC-MSCs proliferation and suppress hUC-MSCs spontaneous osteogenic differentiation. HDACis can affect histone H3 lysine 9 or 14 acetylation and histone H3 lysine 4 dimethylation, thus increasing the mRNA expression of pluripotent and proliferative genes and suppressing the spontaneous differentiation of hUC-MSCs.
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PMID:Role of histone deacetylase inhibitors in the aging of human umbilical cord mesenchymal stem cells. 2356 18


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