Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.24.35 (matrix metalloproteinase 9)
 2,207 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

GH increases linear growth in children with chronic renal failure, but the response remains suboptimal in some patients. Some of the factors that may explain the poor response to GH include high doses of calcitriol and exogenous calcium loading to prevent hyperphosphatemia. High doses of exogenous calcium adversely affect chondrocyte proliferation and delay mineralization in the growth plate of rats with renal failure; bone histomorphometric changes in these animals are comparable to adynamic bone. To evaluate GH effects on adynamic bone in renal failure, 48 weanling rats underwent sham nephrectomy (Intact-Control) or 5/6 nephrectomy (Nx). Nx animals were fed a high-calcium diet (Nx-Ca(2+)) to induce adynamic bone. After 4 wk, the Nx-Ca(2+) animals were treated with GH (Nx-Ca(2+) + GH), calcitriol (Nx-Ca(2+) + D), or a combination of GH and calcitriol (Nx-Ca(2+)GH + D) for 2 wk. Serum intact PTH and IGF-I levels did not differ among all nephrectomized groups given high calcium. GH did not increase body length or tibial length at the end of study period. In the proximal tibia, the width of the growth plate and the growth plate architecture did not improve with GH. There was a decline in histone-4 expression, IGF-I protein, IGF binding protein-3, and bone morphogenetic protein-7 staining and a mild increase in IGF-I receptor, GH receptor, and gelatinase B expression in the Nx-Ca(2+) + GH group when compared with the Intact-Control group. Calcitriol blunted some of the mitogenic effects of GH in the growth plate. Thus, there was a poor response to GH therapy in calcium-loaded animals with renal failure.
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PMID:Growth hormone therapy in calcium-loaded rats with renal failure. 1504 75

The aim of the present study is to evaluate the proliferation- and migration-enhancing effects of ginseng and its component, ginsenoside (Rg1) on RSC96 Schwann cells. We investigated the molecular signaling pathways, which include: (1) survival signaling, IGFs-IGFIR-Akt-Bcl2 and proliferative signaling, cell cycle factors and mitogen-activated protein kinase (MAPK) pathways, (2) migrating and anti-scar signaling, FGF-2-uPA-MMPs.We treated RSC96 cells with different concentrations (100, 200, 300, 400, 500 microg ml(-1)) of ginseng and its constituent, Rg1 (5, 10, 15, 20, 25 microg ml(-1)). We observed a proliferative effect in a dose-dependent manner by PCNA western blotting assay, MTT assay, and wound healing test. Furthermore, we also found in the results of western blotting assay, ginseng and Rg1 enhance protein expression of IGF-I pathway regulators, cell cycle controlling proteins, and MAPK signaling pathways to promote the cell proliferation. In addition, ginseng and Rg1 also stimulated the FGF-2-uPA-MMP 9 migrating pathway to enhance the migration of RSC96 Schwann cells. Using MAPK chemical inhibitors, U0126, SB203580, and SP600125, the proliferative effects of ginseng and Rg1 on RSC96 cells were identified to be MAPK signaling-dependent. On the basis of the results, applying appropriate doses of ginseng and Rg1 with biomedical materials would be a potential approach for enhancing neuron regeneration.
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PMID:Proliferation- and migration-enhancing effects of ginseng and ginsenoside Rg1 through IGF-I- and FGF-2-signaling pathways on RSC96 Schwann cells. 1932 80

This study evaluates the proliferative and migrative effects of dangshen on RSC96, Schwann cells. We investigated the molecular signaling pathways, which include: (1) survival signaling, IGFs-IGFIR-Akt-Bcl2 and proliferative signaling, cell cycle factors and MAPK pathways. (2) migrate and anti-scar signaling, FGF-2-uPA-MMPs. After treatment with different concentrations (20 microg/ml, 40 microg/ml, 60 microg/ml, 80 microg/ml, and 100 microg/ml) of dangshen. We observed a dose dependent proliferative effect using PCNA Western blotting assay, MTT assay and the wound healing test. We also found that dangshen stimulates the protein expressions of IGF-I pathway regulators, cell cycle controlling proteins and excites the MAPK signaling pathway regulators ERK and P38. Dangshen even stimulates the FGF-2-uPA-MMP 9 migration pathway in RSC 96 Schwann cells. Using MAPK chemical inhibitors, U0126, SB203580, and SP600125, the proliferative effects of dangshen on RSC 96 cells were identified to be ERK- and P38- dependent. Based on these results, applying an appropriate dose of dangshen with biomedical materials would be a potential approach for enhancing neuron regeneration.
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PMID:Dangshen (Codonopsis pilosula) activates IGF-I and FGF-2 pathways to induce proliferation and migration effects in RSC96 Schwann cells. 2038 31