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10.1113/EP085794 http://scihub22266oqcxt.onion/10.1113/EP085794 C5600886!5600886!27859785     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Exp+Physiol 2017 ; 102 (2): 139-53 Nephropedia Template TP {{tp|p=27859785|t=2017. Increased monocyte derived reactive oxygen species in type 2 diabetes: Role of endoplasmic reticulum stress |pdf=|usr=}}{{27859785}} gab.com Text Increased monocyte derived reactive oxygen species in type 2 diabetes: Role of endoplasmic reticulum stress JO: Exp Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27859785 #FOAvip Recent evidence suggests that exposure of human monocytes to glucolipotoxic media to mimic the composition of plasma of patients with type 2 diabetes (T2D) results in the induction of endoplasmic reticulum stress markers and formation of reactive oxygen species (ROS). The extent to which these findings translate to patients with T2D remains unclear. Thus, we first measured ROS (dihydroethidium fluorescence) in peripheral blood mononuclear cells (PBMCs) from whole blood of T2D patients (n=8) and compared to age matched healthy controls (n=8). T2D patients exhibited greater basal intracellular ROS (mean±SD, +3.4±1.4 fold; p<0.05) compared to controls. Next, increased ROS in PBMCs isolated from T2D patients was partially recapitulated in cultured human monocytes (THP-1 cells) exposed to plasma from T2D patients for 36 hours (+1.3±0.08 fold vs. plasma from controls; p<0.05). In addition, we found that increased ROS formation in THP-1 cells treated with T2D plasma was NADPH oxidase-derived and led to increased endothelial cell adhesion (+1.8±0.5 fold; p<0.05) and lipid uptake (+1.3±0.3 fold; p<0.05). Notably, we found that T2D plasma-induced monocyte ROS and downstream functional effects were abolished by treating cells with tauroursodeoxycholic acid, a chemical chaperone known to inhibit ER stress. Collectively, these data indicate that monocyte ROS production with T2D can be, in part, attributed to signals from the circulating environment. Furthermore, an interplay between ER stress and NADPH oxidase activity contributes to ROS production and may be a mechanism mediating endothelial cell adhesion and foam cell formation in T2D. Twit Text FOAVip Increased monocyte derived reactive oxygen species in type 2 diabetes: Role of endoplasmic reticulum stress ????Exp Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27859785 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27859785 #FOAvip English Wikipedia <ref>{{Cite pmid|27859785}}</ref> Increased monocyte derived reactive oxygen species in type 2 diabetes: Role of endoplasmic reticulum stress #MMPMID27859785 Restaino RM; Deo SH; Parrish AR; Fadel PJ; Padilla J Exp Physiol 2017[Feb]; 102 (2): 139-53 PMID27859785show ga Recent evidence suggests that exposure of human monocytes to glucolipotoxic media to mimic the composition of plasma of patients with type 2 diabetes (T2D) results in the induction of endoplasmic reticulum stress markers and formation of reactive oxygen species (ROS). The extent to which these findings translate to patients with T2D remains unclear. Thus, we first measured ROS (dihydroethidium fluorescence) in peripheral blood mononuclear cells (PBMCs) from whole blood of T2D patients (n=8) and compared to age matched healthy controls (n=8). T2D patients exhibited greater basal intracellular ROS (mean±SD, +3.4±1.4 fold; p<0.05) compared to controls. Next, increased ROS in PBMCs isolated from T2D patients was partially recapitulated in cultured human monocytes (THP-1 cells) exposed to plasma from T2D patients for 36 hours (+1.3±0.08 fold vs. plasma from controls; p<0.05). In addition, we found that increased ROS formation in THP-1 cells treated with T2D plasma was NADPH oxidase-derived and led to increased endothelial cell adhesion (+1.8±0.5 fold; p<0.05) and lipid uptake (+1.3±0.3 fold; p<0.05). Notably, we found that T2D plasma-induced monocyte ROS and downstream functional effects were abolished by treating cells with tauroursodeoxycholic acid, a chemical chaperone known to inhibit ER stress. Collectively, these data indicate that monocyte ROS production with T2D can be, in part, attributed to signals from the circulating environment. Furthermore, an interplay between ER stress and NADPH oxidase activity contributes to ROS production and may be a mechanism mediating endothelial cell adhesion and foam cell formation in T2D. äIncreased monocyte derived reactive oxygen species in type 2 diabetes:(epmc).pdf DeepDyve Pubget Overpricing