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10.1186/s12931-017-0603-0 http://scihub22266oqcxt.onion/10.1186/s12931-017-0603-0 C5483271!5483271!28646872     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Respir+Res 2017 ; 18 (ä): ä Nephropedia Template TP {{tp|p=28646872|t=2017. Role of P2X7R in the development and progression of pulmonary hypertension |pdf=|usr=}}{{28646872}} gab.com Text Role of P2X7R in the development and progression of pulmonary hypertension JO: Respir Res http://www.kidney.de/pget.php?&tw=1&pmid=28646872 #FOAvip Background: Pulmonary arterial hypertension (PAH) is a devastating disease that lacks sufficient treatment. Studies have shown that the Nod-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome contributes to PAH pathogenesis, but the role of the upstream molecular P2X7 receptor (P2X7R) has remained unexplored. We investigated the role of P2X7R in the pathogenesis of PAH. Methods and results: PH was induced by a single subcutaneous injection of monocrotaline (MCT) (60 mg/kg) on left pneumonectomised Sprague-Dawley rats, as validated by significant increases in pulmonary artery pressure and vessel wall thickness. Marked P2X7R was detected by predominant PA immunostaining in lungs from PH rats. Western blot revealed a significant increase in the protein levels of P2X7R as well as NLRP3 and caspase-1 in the diseased lung tissue compared with normal tissue. The rats received A-740003 (a selective P2X7 receptor antagonist, 30 mg/kg) daily starting from 1 week before or 2 weeks after MCT injection. Consequently, A-740003 reversed the NLRP3 inflammasome upregulation, significantly decreased the mean right ventricular (RV) pressure and RV hypertrophy, and reversed pulmonary arterial remodelling 4 weeks after MCT injection, as both a pretreatment and rescue intervention. Notably, A-740003 significantly reduced macrophage and pro-inflammatory cytokine levels, as measured via bronchoalveolar lavage. The recruitment of macrophages as well as collagen fibre deposition in the perivascular areas were also reduced, as confirmed by histological staining. Conclusions: P2X7R contributes to the pathogenesis of PH, probably in association with activation of the NLRP3 inflammasome. Blockade of P2X7R might be applied as a novel therapeutic approach for the treatment of PAH. Electronic supplementary material: The online version of this article (doi:10.1186/s12931-017-0603-0) contains supplementary material, which is available to authorized users. Twit Text FOAVip Role of P2X7R in the development and progression of pulmonary hypertension ????Respir Res http://www.kidney.de/pget.php?&tw=1&pmid=28646872 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28646872 #FOAvip English Wikipedia <ref>{{Cite pmid|28646872}}</ref> Role of P2X7R in the development and progression of pulmonary hypertension #MMPMID28646872 Yin J; You S; Liu H; Chen L; Zhang C; Hu H; Xue M; Cheng W; Wang Y; Li X; Shi Y; Li N; Yan S; Li X Respir Res 2017[]; 18 (ä): ä PMID28646872show ga Background: Pulmonary arterial hypertension (PAH) is a devastating disease that lacks sufficient treatment. Studies have shown that the Nod-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome contributes to PAH pathogenesis, but the role of the upstream molecular P2X7 receptor (P2X7R) has remained unexplored. We investigated the role of P2X7R in the pathogenesis of PAH. Methods and results: PH was induced by a single subcutaneous injection of monocrotaline (MCT) (60 mg/kg) on left pneumonectomised Sprague-Dawley rats, as validated by significant increases in pulmonary artery pressure and vessel wall thickness. Marked P2X7R was detected by predominant PA immunostaining in lungs from PH rats. Western blot revealed a significant increase in the protein levels of P2X7R as well as NLRP3 and caspase-1 in the diseased lung tissue compared with normal tissue. The rats received A-740003 (a selective P2X7 receptor antagonist, 30 mg/kg) daily starting from 1 week before or 2 weeks after MCT injection. Consequently, A-740003 reversed the NLRP3 inflammasome upregulation, significantly decreased the mean right ventricular (RV) pressure and RV hypertrophy, and reversed pulmonary arterial remodelling 4 weeks after MCT injection, as both a pretreatment and rescue intervention. Notably, A-740003 significantly reduced macrophage and pro-inflammatory cytokine levels, as measured via bronchoalveolar lavage. The recruitment of macrophages as well as collagen fibre deposition in the perivascular areas were also reduced, as confirmed by histological staining. Conclusions: P2X7R contributes to the pathogenesis of PH, probably in association with activation of the NLRP3 inflammasome. Blockade of P2X7R might be applied as a novel therapeutic approach for the treatment of PAH. Electronic supplementary material: The online version of this article (doi:10.1186/s12931-017-0603-0) contains supplementary material, which is available to authorized users. äRole of P2X7R in the development and progression of pulmonary hyperten(epmc).pdf DeepDyve Pubget Overpricing