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10.1007/s00011-013-0653-9

http://scihub22266oqcxt.onion/10.1007/s00011-013-0653-9
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23934071!ä!23934071

suck abstract from ncbi


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pmid23934071      Inflamm+Res 2013 ; 62 (11): 961-70
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  • Inhibition of TRPM7 channels prevents proliferation and differentiation of human lung fibroblasts #MMPMID23934071
  • Yu M; Huang C; Huang Y; Wu X; Li X; Li J
  • Inflamm Res 2013[Nov]; 62 (11): 961-70 PMID23934071show ga
  • OBJECTIVE: Transient receptor potential melastatin 7 (TRPM7) is involved in both normal physiological processes and pathology of various diseases. The purpose of this study was to explore the function and underlying mechanisms of TRPM7 channels in human lung fibroblast (MRC5) proliferation and differentiation induced by transforming growth factor beta1 (TGF-beta1) in vitro. MATERIALS AND METHODS: We determined the expression of TRPM7 in MRC5 cells in response to TGF-beta1 treatment in vitro. Chemical inhibitors (Gd(3+) and 2-APB) and specific siRNA for TRPM7 were used to study the role of TRPM7 in MRC5 cell proliferation and differentiation. The phosphorylation of Akt was determined by Western blotting. RESULTS: The expression of TRPM7 was significantly potentiated in response to TGF-beta1. Co-incubation of MRC5 cells with Gd(3+), 2-APB or TRPM7-siRNA decreased cell proliferation and differentiation. Furthermore, we found that suppression of TRPM7 channels also reduced the p-Akt in MRC5 cells induced by TGF-beta1. We conclude that suppression of TRPM7 channels may decrease fibroblast proliferation and differentiation stimulated by TGF-beta1 in vitro and this is associated with Akt phosphorylation.
  • |Cell Cycle/drug effects[MESH]
  • |Cell Differentiation/drug effects[MESH]
  • |Cell Line[MESH]
  • |Cell Proliferation/drug effects[MESH]
  • |Fibroblasts/*cytology/drug effects/metabolism[MESH]
  • |Gene Silencing[MESH]
  • |Humans[MESH]
  • |Lung/cytology[MESH]
  • |MCF-7 Cells[MESH]
  • |Phosphatidylinositol 3-Kinases/metabolism[MESH]
  • |Protein Serine-Threonine Kinases[MESH]
  • |Proto-Oncogene Proteins c-akt/metabolism[MESH]
  • |RNA, Small Interfering/genetics[MESH]
  • |TRPM Cation Channels/*antagonists & inhibitors/genetics/metabolism[MESH]


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