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10.1371/journal.pone.0123432 http://scihub22266oqcxt.onion/10.1371/journal.pone.0123432 C4401536!4401536 !25884983     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25884983 &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 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 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\25884983 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       PLoS+One 2015 ; 10 (4 ): e0123432 Nephropedia Template TP {{tp|p=25884983 |t=2015. Store-operated Ca2+ entry plays a role in HMGB1-induced vascular endothelial cell hyperpermeability |pdf=|usr=}}{{25884983 }} gab.com Text Store-operated Ca2+ entry plays a role in HMGB1-induced vascular endothelial cell hyperpermeability JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=25884983 #FOAvip AIMS: Endothelial dysfunction, including increased endothelial permeability, is considered an early marker for atherosclerosis. High-mobility group box 1 protein (HMGB1) and extracellular Ca2+ entry, primarily mediated through store-operated Ca2+ entry (SOCE), are known to be involved in increasing endothelial permeability. The aim of this study was to clarify how HMGB1 could lead to endothelia hyperpermeability. METHODS AND RESULTS: We have shown that human vascular endothelial cell permeability is increased, while transendothelial electrical resistance and VE-cadherin expression were reduced by HMGB1 treatment. Two SOCE inhibitors and knockdown of stromal interaction molecule 1 (STIM1), a Ca2+ sensor mediating SOCE, inhibited the HMGB1-induced influx of Ca2+ and Src activation followed by significant suppression of endothelial permeability. Moreover, knockdown of Orai1, an essential pore-subunit of SOCE channels, decreased HMGB1-induced endothelial hyperpermeability. CONCLUSIONS: These data suggest that SOCE, acting via STIM1, might be the predominant mechanism of Ca2+ entry in the modulation of endothelial cell permeability. STIM1 may thus represent a possible new therapeutic target against atherosclerosis. Twit Text FOAVip Store-operated Ca2+ entry plays a role in HMGB1-induced vascular endothelial cell hyperpermeability ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=25884983 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25884983 #FOAvip English Wikipedia <ref>{{Cite pmid|25884983 }}</ref> Store-operated Ca2+ entry plays a role in HMGB1-induced vascular endothelial cell hyperpermeability #MMPMID25884983 Zou M ; Dong H ; Meng X ; Cai C ; Li C ; Cai S ; Xue Y PLoS One 2015[]; 10 (4 ): e0123432 PMID25884983 show ga AIMS: Endothelial dysfunction, including increased endothelial permeability, is considered an early marker for atherosclerosis. High-mobility group box 1 protein (HMGB1) and extracellular Ca2+ entry, primarily mediated through store-operated Ca2+ entry (SOCE), are known to be involved in increasing endothelial permeability. The aim of this study was to clarify how HMGB1 could lead to endothelia hyperpermeability. METHODS AND RESULTS: We have shown that human vascular endothelial cell permeability is increased, while transendothelial electrical resistance and VE-cadherin expression were reduced by HMGB1 treatment. Two SOCE inhibitors and knockdown of stromal interaction molecule 1 (STIM1), a Ca2+ sensor mediating SOCE, inhibited the HMGB1-induced influx of Ca2+ and Src activation followed by significant suppression of endothelial permeability. Moreover, knockdown of Orai1, an essential pore-subunit of SOCE channels, decreased HMGB1-induced endothelial hyperpermeability. CONCLUSIONS: These data suggest that SOCE, acting via STIM1, might be the predominant mechanism of Ca2+ entry in the modulation of endothelial cell permeability. STIM1 may thus represent a possible new therapeutic target against atherosclerosis. |Aorta/cytology/drug effects/metabolism [MESH] |Cadherins/metabolism [MESH] |Calcium Channels/metabolism [MESH] |Calcium Signaling/drug effects/physiology [MESH] |Calcium/*metabolism [MESH] |Endothelium, Vascular/cytology/drug effects/*metabolism [MESH] |HMGB1 Protein/*pharmacology [MESH] |Human Umbilical Vein Endothelial Cells/cytology/drug effects/*metabolism [MESH] |Humans [MESH] |Membrane Proteins/metabolism [MESH] |Neoplasm Proteins/metabolism [MESH] |Permeability [MESH]Store-operated Ca2+ entry plays a role in HMGB1-induced vascular endot(epmc).pdf DeepDyve Pubget Overpricing