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10.1007/s00424-017-1989-8 http://scihub22266oqcxt.onion/10.1007/s00424-017-1989-8 C5590033!5590033 !28497275     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 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\28497275 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Pflugers+Arch 2017 ; 469 (10 ): 1287-1299 Nephropedia Template TP {{tp|p=28497275 |t=2017. Na (+)/Ca(2+) exchangers and Orai channels jointly refill endoplasmic reticulum (ER) Ca(2+) via ER nanojunctions in vascular endothelial cells |pdf=|usr=}}{{28497275 }} gab.com Text Na (+)/Ca(2+) exchangers and Orai channels jointly refill endoplasmic reticulum (ER) Ca(2+) via ER nanojunctions in vascular endothelial cells JO: Pflugers Arch http://www.kidney.de/pget.php?&tw=1&pmid=28497275 #FOAvip We investigated the role of Na(+)/ Ca(2+) exchange (NCX) in the refilling of endoplasmic reticulum (ER) Ca(2+) in vascular endothelial cells under various conditions of cell stimulation and plasma membrane (PM) polarization. Better understanding of the mechanisms behind basic ER Ca(2+) content regulation is important, since current hypotheses on the possible ultimate causes of ER stress point to deterioration of the Ca(2+) transport mechanism to/from ER itself. We measured [Ca(2+)](i) temporal changes by Fura-2 fluorescence under experimental protocols that inhibit a host of transporters (NCX, Orai, non-selective transient receptor potential canonical (TRPC) channels, sarco/endoplasmic reticulum Ca(2+) ATPase (SERCA), Na(+)/ K(+) ATPase (NKA)) involved in the Ca(2+) communication between the extracellular space and the ER. Following histamine-stimulated ER Ca(2+) release, blockade of NCX Ca(2+)-influx mode (by 10 ?M KB-R7943) diminished the ER refilling capacity by about 40%, while in Orai1 dominant negative-transfected cells NCX blockade attenuated ER refilling by about 60%. Conversely, inhibiting the ouabain sensitive NKA (10 nM ouabain), which may be localized in PM-ER junctions, increased the ER Ca(2+) releasable fraction by about 20%, thereby supporting the hypothesis that this process of privileged ER refilling is junction-mediated. Junctions were observed in the cell ultrastructure and their main parameters of membrane separation and linear extension were (9.6 ± 3.8) nm and (128 ± 63) nm, respectively. Our findings point to a process of privileged refilling of the ER, in which NCX and store-operated Ca(2+) entry via the stromal interaction molecule (STIM)-Orai system are the sole protagonists. These results shed light on the molecular machinery involved in the function of a previously hypothesized subplasmalemmal Ca(2+) control unit during ER refilling with extracellular Ca(2+). Twit Text FOAVip Na (+)/Ca(2+) exchangers and Orai channels jointly refill endoplasmic reticulum (ER) Ca(2+) via ER nanojunctions in vascular endothelial cells ????Pflugers Arch http://www.kidney.de/pget.php?&tw=1&pmid=28497275 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28497275 #FOAvip English Wikipedia <ref>{{Cite pmid|28497275 }}</ref> Na (+)/Ca(2+) exchangers and Orai channels jointly refill endoplasmic reticulum (ER) Ca(2+) via ER nanojunctions in vascular endothelial cells #MMPMID28497275 Di Giuro CML ; Shrestha N ; Malli R ; Groschner K ; van Breemen C ; Fameli N Pflugers Arch 2017[Oct]; 469 (10 ): 1287-1299 PMID28497275 show ga We investigated the role of Na(+)/ Ca(2+) exchange (NCX) in the refilling of endoplasmic reticulum (ER) Ca(2+) in vascular endothelial cells under various conditions of cell stimulation and plasma membrane (PM) polarization. Better understanding of the mechanisms behind basic ER Ca(2+) content regulation is important, since current hypotheses on the possible ultimate causes of ER stress point to deterioration of the Ca(2+) transport mechanism to/from ER itself. We measured [Ca(2+)](i) temporal changes by Fura-2 fluorescence under experimental protocols that inhibit a host of transporters (NCX, Orai, non-selective transient receptor potential canonical (TRPC) channels, sarco/endoplasmic reticulum Ca(2+) ATPase (SERCA), Na(+)/ K(+) ATPase (NKA)) involved in the Ca(2+) communication between the extracellular space and the ER. Following histamine-stimulated ER Ca(2+) release, blockade of NCX Ca(2+)-influx mode (by 10 ?M KB-R7943) diminished the ER refilling capacity by about 40%, while in Orai1 dominant negative-transfected cells NCX blockade attenuated ER refilling by about 60%. Conversely, inhibiting the ouabain sensitive NKA (10 nM ouabain), which may be localized in PM-ER junctions, increased the ER Ca(2+) releasable fraction by about 20%, thereby supporting the hypothesis that this process of privileged ER refilling is junction-mediated. Junctions were observed in the cell ultrastructure and their main parameters of membrane separation and linear extension were (9.6 ± 3.8) nm and (128 ± 63) nm, respectively. Our findings point to a process of privileged refilling of the ER, in which NCX and store-operated Ca(2+) entry via the stromal interaction molecule (STIM)-Orai system are the sole protagonists. These results shed light on the molecular machinery involved in the function of a previously hypothesized subplasmalemmal Ca(2+) control unit during ER refilling with extracellular Ca(2+). |Calcium Channels/metabolism [MESH] |Calcium Signaling/physiology [MESH] |Calcium/*metabolism [MESH] |Cell Membrane/metabolism [MESH] |Endoplasmic Reticulum/*metabolism [MESH] |Endothelial Cells/*metabolism [MESH] |Humans [MESH] |Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism [MESH]Na (+)/Ca(2+) exchangers and Orai channels jointly refill endoplasmic (epmc).pdf DeepDyve Pubget Overpricing