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10.1158/0008-5472.CAN-14-1616 http://scihub22266oqcxt.onion/10.1158/0008-5472.CAN-14-1616 C4383705!4383705!25634211     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25634211.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Cancer+Res 2015 ; 75 (7): 1244-54 Nephropedia Template TP {{tp|p=25634211|t=2015. Tumor endothelial cells with distinct patterns of TGF?-driven endothelial-to-mesenchymal transition |pdf=|usr=}}{{25634211}} gab.com Text Tumor endothelial cells with distinct patterns of TGF -driven endothelial-to-mesenchymal transition JO: Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=25634211 #FOAvip Endothelial-to-mesenchymal transition (EndMT) occurs during development and underlies the pathophysiology of multiple diseases. In tumors, unscheduled EndMT generates cancer-associated myofibroblasts that fuel inflammation and fibrosis, and may contribute to vascular dysfunction that promotes tumor progression. We report that freshly isolated subpopulations of tumor-specific endothelial cells (TEC) from a spontaneous mammary tumor model undergo distinct forms of EndMT in response to TGF? stimulation. Whereas some TEC strikingly up-regulate alpha smooth muscle actin (SMA), a principal marker of EndMT and activated myofibroblasts, counterpart normal mammary gland endothelial cells (NEC) showed little change in SMA expression after TGF? treatment. Compared with NEC, SMA+ TEC were 40 % less motile in wound healing assays and formed more stable vascular-like networks in vitro when challenged with TGF?. Lineage tracing using ZsGreenCdh5-Cre reporter mice confirmed that only a fraction of vessels in breast tumors contain SMA+ TEC, suggesting that not all endothelial cells (EC) respond identically to TGF? in vivo. Indeed, examination of 84 TGF?-regulated target genes revealed entirely different genetic signatures in TGF?-stimulated NEC and TEC cultures. Finally, we found that basic FGF (bFGF) exerts potent inhibitory effects on many TGF?-regulated genes but operates in tandem with TGF? to up-regulate others. EC challenged with TGF? secrete bFGF which blocks SMA expression in secondary cultures suggesting a cell-autonomous or lateral-inhibitory mechanism for impeding mesenchymal differentiation. Together, our results suggest that TGF?-driven EndMT produces a spectrum of EC phenotypes with different functions that could underlie the plasticity and heterogeneity of the tumor vasculature. Twit Text FOAVip Tumor endothelial cells with distinct patterns of TGF -driven endothelial-to-mesenchymal transition ????Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=25634211 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25634211 #FOAvip English Wikipedia <ref>{{Cite pmid|25634211}}</ref> Tumor endothelial cells with distinct patterns of TGF?-driven endothelial-to-mesenchymal transition #MMPMID25634211 Xiao L; Kim DJ; Davis CL; McCann JV; Dunleavey JM; Vanderlinden A; Xu N; Pattenden SG; Frye SV; Xu X; Onaitis M; Monaghan-Benson E; Burridge K; Dudley AC Cancer Res 2015[Apr]; 75 (7): 1244-54 PMID25634211show ga Endothelial-to-mesenchymal transition (EndMT) occurs during development and underlies the pathophysiology of multiple diseases. In tumors, unscheduled EndMT generates cancer-associated myofibroblasts that fuel inflammation and fibrosis, and may contribute to vascular dysfunction that promotes tumor progression. We report that freshly isolated subpopulations of tumor-specific endothelial cells (TEC) from a spontaneous mammary tumor model undergo distinct forms of EndMT in response to TGF? stimulation. Whereas some TEC strikingly up-regulate alpha smooth muscle actin (SMA), a principal marker of EndMT and activated myofibroblasts, counterpart normal mammary gland endothelial cells (NEC) showed little change in SMA expression after TGF? treatment. Compared with NEC, SMA+ TEC were 40 % less motile in wound healing assays and formed more stable vascular-like networks in vitro when challenged with TGF?. Lineage tracing using ZsGreenCdh5-Cre reporter mice confirmed that only a fraction of vessels in breast tumors contain SMA+ TEC, suggesting that not all endothelial cells (EC) respond identically to TGF? in vivo. Indeed, examination of 84 TGF?-regulated target genes revealed entirely different genetic signatures in TGF?-stimulated NEC and TEC cultures. Finally, we found that basic FGF (bFGF) exerts potent inhibitory effects on many TGF?-regulated genes but operates in tandem with TGF? to up-regulate others. EC challenged with TGF? secrete bFGF which blocks SMA expression in secondary cultures suggesting a cell-autonomous or lateral-inhibitory mechanism for impeding mesenchymal differentiation. Together, our results suggest that TGF?-driven EndMT produces a spectrum of EC phenotypes with different functions that could underlie the plasticity and heterogeneity of the tumor vasculature. äTumor endothelial cells with distinct patterns of TGF?-driven endothel(epmc).pdf DeepDyve Pubget Overpricing