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10.1161/CIRCRESAHA.115.304382 http://scihub22266oqcxt.onion/10.1161/CIRCRESAHA.115.304382 C4810682!4810682 !25091710     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 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 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 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 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\25091710 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Circ+Res 2014 ; 115 (8 ): 709-20 Nephropedia Template TP {{tp|p=25091710 |t=2014. FOXF1 transcription factor is required for formation of embryonic vasculature by regulating VEGF signaling in endothelial cells |pdf=|usr=}}{{25091710 }} gab.com Text FOXF1 transcription factor is required for formation of embryonic vasculature by regulating VEGF signaling in endothelial cells JO: Circ Res http://www.kidney.de/pget.php?&tw=1&pmid=25091710 #FOAvip RATIONALE: Inactivating mutations in the Forkhead Box transcription factor F1 (FOXF1) gene locus are frequently found in patients with alveolar capillary dysplasia with misalignment of pulmonary veins, a lethal congenital disorder, which is characterized by severe abnormalities in the respiratory, cardiovascular, and gastrointestinal systems. In mice, haploinsufficiency of the Foxf1 gene causes alveolar capillary dysplasia and developmental defects in lung, intestinal, and gall bladder morphogenesis. OBJECTIVE: Although FOXF1 is expressed in multiple mesenchyme-derived cell types, cellular origins and molecular mechanisms of developmental abnormalities in FOXF1-deficient mice and patients with alveolar capillary dysplasia with misalignment of pulmonary veins remain uncharacterized because of lack of mouse models with cell-restricted inactivation of the Foxf1 gene. In the present study, the role of FOXF1 in endothelial cells was examined using a conditional knockout approach. METHODS AND RESULTS: A novel mouse line harboring Foxf1-floxed alleles was generated by homologous recombination. Tie2-Cre and Pdgfb-CreER transgenes were used to delete Foxf1 from endothelial cells. FOXF1-deficient embryos exhibited embryonic lethality, growth retardation, polyhydramnios, cardiac ventricular hypoplasia, and vascular abnormalities in the lung, placenta, yolk sac, and retina. Deletion of FOXF1 from endothelial cells reduced endothelial proliferation, increased apoptosis, inhibited vascular endothelial growth factor signaling, and decreased expression of endothelial genes critical for vascular development, including vascular endothelial growth factor receptors Flt1 and Flk1, Pdgfb, Pecam1, CD34, integrin ?3, ephrin B2, Tie2, and the noncoding RNA Fendrr. Chromatin immunoprecipitation assay demonstrated that Flt1, Flk1, Pdgfb, Pecam1, and Tie2 genes are direct transcriptional targets of FOXF1. CONCLUSIONS: FOXF1 is required for the formation of embryonic vasculature by regulating endothelial genes critical for vascular development and vascular endothelial growth factor signaling. Twit Text FOAVip FOXF1 transcription factor is required for formation of embryonic vasculature by regulating VEGF signaling in endothelial cells ????Circ Res http://www.kidney.de/pget.php?&tw=1&pmid=25091710 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25091710 #FOAvip English Wikipedia <ref>{{Cite pmid|25091710 }}</ref> FOXF1 transcription factor is required for formation of embryonic vasculature by regulating VEGF signaling in endothelial cells #MMPMID25091710 Ren X ; Ustiyan V ; Pradhan A ; Cai Y ; Havrilak JA ; Bolte CS ; Shannon JM ; Kalin TV ; Kalinichenko VV Circ Res 2014[Sep]; 115 (8 ): 709-20 PMID25091710 show ga RATIONALE: Inactivating mutations in the Forkhead Box transcription factor F1 (FOXF1) gene locus are frequently found in patients with alveolar capillary dysplasia with misalignment of pulmonary veins, a lethal congenital disorder, which is characterized by severe abnormalities in the respiratory, cardiovascular, and gastrointestinal systems. In mice, haploinsufficiency of the Foxf1 gene causes alveolar capillary dysplasia and developmental defects in lung, intestinal, and gall bladder morphogenesis. OBJECTIVE: Although FOXF1 is expressed in multiple mesenchyme-derived cell types, cellular origins and molecular mechanisms of developmental abnormalities in FOXF1-deficient mice and patients with alveolar capillary dysplasia with misalignment of pulmonary veins remain uncharacterized because of lack of mouse models with cell-restricted inactivation of the Foxf1 gene. In the present study, the role of FOXF1 in endothelial cells was examined using a conditional knockout approach. METHODS AND RESULTS: A novel mouse line harboring Foxf1-floxed alleles was generated by homologous recombination. Tie2-Cre and Pdgfb-CreER transgenes were used to delete Foxf1 from endothelial cells. FOXF1-deficient embryos exhibited embryonic lethality, growth retardation, polyhydramnios, cardiac ventricular hypoplasia, and vascular abnormalities in the lung, placenta, yolk sac, and retina. Deletion of FOXF1 from endothelial cells reduced endothelial proliferation, increased apoptosis, inhibited vascular endothelial growth factor signaling, and decreased expression of endothelial genes critical for vascular development, including vascular endothelial growth factor receptors Flt1 and Flk1, Pdgfb, Pecam1, CD34, integrin ?3, ephrin B2, Tie2, and the noncoding RNA Fendrr. Chromatin immunoprecipitation assay demonstrated that Flt1, Flk1, Pdgfb, Pecam1, and Tie2 genes are direct transcriptional targets of FOXF1. CONCLUSIONS: FOXF1 is required for the formation of embryonic vasculature by regulating endothelial genes critical for vascular development and vascular endothelial growth factor signaling. |*Signal Transduction [MESH] |Animals [MESH] |Apoptosis/genetics [MESH] |Base Sequence [MESH] |Blood Vessels/embryology/*metabolism [MESH] |Blotting, Western [MESH] |Cell Line [MESH] |Cells, Cultured [MESH] |Embryo, Mammalian/cytology/embryology/metabolism [MESH] |Endothelial Cells/*metabolism [MESH] |Forkhead Transcription Factors/genetics/*metabolism [MESH] |Gene Expression Regulation, Developmental [MESH] |Humans [MESH] |Immunohistochemistry [MESH] |Lung/blood supply/embryology/metabolism [MESH] |Mesoderm/cytology/metabolism [MESH] |Mice [MESH] |Mice, 129 Strain [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Mice, Transgenic [MESH] |Molecular Sequence Data [MESH] |Reverse Transcriptase Polymerase Chain Reaction [MESH] |Sequence Homology, Nucleic Acid [MESH]FOXF1 transcription factor is required for formation of embryonic vasc(epmc).pdf DeepDyve Pubget Overpricing