Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1038/nature13839 http://scihub22266oqcxt.onion/10.1038/nature13839 C4214889!4214889 !25317562     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25317562 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 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\25317562 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Nature 2014 ; 514 (7524 ): 585-90 Nephropedia Template TP {{tp|p=25317562 |t=2014. Mesenchymal-endothelial transition contributes to cardiac neovascularization |pdf=|usr=}}{{25317562 }} gab.com Text Mesenchymal-endothelial transition contributes to cardiac neovascularization JO: Nature http://www.kidney.de/pget.php?&tw=1&pmid=25317562 #FOAvip Endothelial cells contribute to a subset of cardiac fibroblasts by undergoing endothelial-to-mesenchymal transition, but whether cardiac fibroblasts can adopt an endothelial cell fate and directly contribute to neovascularization after cardiac injury is not known. Here, using genetic fate map techniques, we demonstrate that cardiac fibroblasts rapidly adopt an endothelial-cell-like phenotype after acute ischaemic cardiac injury. Fibroblast-derived endothelial cells exhibit anatomical and functional characteristics of native endothelial cells. We show that the transcription factor p53 regulates such a switch in cardiac fibroblast fate. Loss of p53 in cardiac fibroblasts severely decreases the formation of fibroblast-derived endothelial cells, reduces post-infarct vascular density and worsens cardiac function. Conversely, stimulation of the p53 pathway in cardiac fibroblasts augments mesenchymal-to-endothelial transition, enhances vascularity and improves cardiac function. These observations demonstrate that mesenchymal-to-endothelial transition contributes to neovascularization of the injured heart and represents a potential therapeutic target for enhancing cardiac repair. Twit Text FOAVip Mesenchymal-endothelial transition contributes to cardiac neovascularization ????Nature http://www.kidney.de/pget.php?&tw=1&pmid=25317562 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25317562 #FOAvip English Wikipedia <ref>{{Cite pmid|25317562 }}</ref> Mesenchymal-endothelial transition contributes to cardiac neovascularization #MMPMID25317562 Ubil E ; Duan J ; Pillai IC ; Rosa-Garrido M ; Wu Y ; Bargiacchi F ; Lu Y ; Stanbouly S ; Huang J ; Rojas M ; Vondriska TM ; Stefani E ; Deb A Nature 2014[Oct]; 514 (7524 ): 585-90 PMID25317562 show ga Endothelial cells contribute to a subset of cardiac fibroblasts by undergoing endothelial-to-mesenchymal transition, but whether cardiac fibroblasts can adopt an endothelial cell fate and directly contribute to neovascularization after cardiac injury is not known. Here, using genetic fate map techniques, we demonstrate that cardiac fibroblasts rapidly adopt an endothelial-cell-like phenotype after acute ischaemic cardiac injury. Fibroblast-derived endothelial cells exhibit anatomical and functional characteristics of native endothelial cells. We show that the transcription factor p53 regulates such a switch in cardiac fibroblast fate. Loss of p53 in cardiac fibroblasts severely decreases the formation of fibroblast-derived endothelial cells, reduces post-infarct vascular density and worsens cardiac function. Conversely, stimulation of the p53 pathway in cardiac fibroblasts augments mesenchymal-to-endothelial transition, enhances vascularity and improves cardiac function. These observations demonstrate that mesenchymal-to-endothelial transition contributes to neovascularization of the injured heart and represents a potential therapeutic target for enhancing cardiac repair. |*Cell Transdifferentiation [MESH] |*Neovascularization, Physiologic [MESH] |Animals [MESH] |Coronary Vessels/*cytology/*growth & development [MESH] |Endothelial Cells/*cytology [MESH] |Female [MESH] |Fibroblasts/cytology [MESH] |In Vitro Techniques [MESH] |Male [MESH] |Mesoderm/*cytology [MESH] |Mice [MESH] |Myocardial Ischemia/*pathology [MESH]Mesenchymal-endothelial transition contributes to cardiac neovasculari(epmc).pdf DeepDyve Pubget Overpricing