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10.1097/TP.0000000000000762 http://scihub22266oqcxt.onion/10.1097/TP.0000000000000762 C4618723!4618723!25989500     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25989500&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 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 259.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 259.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 259.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Transplantation 2015 ; 99 (11): 2274-84 Nephropedia Template TP {{tp|p=25989500|t=2015. Stimulation of Dopamine D3 Receptor Attenuates Renal Ischemia/Reperfusion Injury via Increased Linkage with G?12 |pdf=|usr=}}{{25989500}} gab.com Text Stimulation of Dopamine D3 Receptor Attenuates Renal Ischemia/Reperfusion Injury via Increased Linkage with G 12 JO: Transplantation http://www.kidney.de/pget.php?&tw=1&pmid=25989500 #FOAvip Background: Renal ischemia reperfusion (I/R) injury causes renal tubular necrosis, apoptosis, and inflammation leading to acute renal dysfunction. Recent studies have revealed that deletion of G?12 mitigates the renal damage due to I/R injury. Our previous study showed that activation of D3R increased its linkage with G?12, and hampered G?12-mediated stimulation of renal sodium transport. In the present study, we used an in-vivo rat model and an in-vitro study of the renal epithelial cell line (NRK52E) to investigate whether or not an increased linkage between D3R and G?12 contributes to the protective effect of D3R on renal I/R injury. Methods: For in-vivo studies, ischemia/reperfusion injury was induced in a rat renal unilateral clamping model. For in-vitro studies, hypoxia/reoxygenation and cold storage/rewarming injuries were performed in NRK52E cells. PD128907, a D3R agonist, or vehicle , was administered 15 min before clamping (or hypoxia) in both the in-vivo or in-vitro studies. Results: In the rat renal unilateral clamping model, pretreatment with PD128907 (0.2 mg/kg, IV) protected against renal I/R injury and increased survival rate during a long-term follow-up after seven days. A decrease in the generation of ROS, apoptosis and inflammation may be involved in the D3R-mediated protection since pretreatment with PD128907 increased renal glutathione and superoxide dismutase levels and decreased malondialdehyde levels in the I/R group. The increase in cytokines (TNF-?, IL-1?, and IL-10) and myeloperoxidase in I/R injured kidney was also prevented with a , simultaneous decrease in the apoptosis of the epithelial cells and expression of apoptosis biomarkers in kidney harvested one day after I/R injury. The increase in the co-immunoprecipitation between D3R and G?12 with D3R stimulation paralleled the observed renal protection from I/R injury. Moreover, in vitro studies showed that transient overexpression of G?12 in the NRK52E cells attenuated the protective effect of PD128907 on H/R injury. The protective effect of PD128907 might be of significance to renal transplantation, since cold storage/rewarming induced injury increased LDH release and decreased cell viability in NRK52E cells. Conversely, in the presence of PD128907, the increased LDH release and decreased cell viability were reversed. Conclusion: These results suggest that activation of D3R, by decreasing G?12-induced renal damage, may exert a protective effect from I/R injury. Twit Text FOAVip Stimulation of Dopamine D3 Receptor Attenuates Renal Ischemia/Reperfusion Injury via Increased Linkage with G 12 ????Transplantation http://www.kidney.de/pget.php?&tw=1&pmid=25989500 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25989500 #FOAvip English Wikipedia <ref>{{Cite pmid|25989500}}</ref> Stimulation of Dopamine D3 Receptor Attenuates Renal Ischemia/Reperfusion Injury via Increased Linkage with G?12 #MMPMID25989500 Wang Z; Guan W; Han Y; Ren H; Tang X; Zhang H; Liu Y; Fu J; He D; Asico LD; Jose PA; Zhou L; Chen L; Zeng C Transplantation 2015[Nov]; 99 (11): 2274-84 PMID25989500show ga Background: Renal ischemia reperfusion (I/R) injury causes renal tubular necrosis, apoptosis, and inflammation leading to acute renal dysfunction. Recent studies have revealed that deletion of G?12 mitigates the renal damage due to I/R injury. Our previous study showed that activation of D3R increased its linkage with G?12, and hampered G?12-mediated stimulation of renal sodium transport. In the present study, we used an in-vivo rat model and an in-vitro study of the renal epithelial cell line (NRK52E) to investigate whether or not an increased linkage between D3R and G?12 contributes to the protective effect of D3R on renal I/R injury. Methods: For in-vivo studies, ischemia/reperfusion injury was induced in a rat renal unilateral clamping model. For in-vitro studies, hypoxia/reoxygenation and cold storage/rewarming injuries were performed in NRK52E cells. PD128907, a D3R agonist, or vehicle , was administered 15 min before clamping (or hypoxia) in both the in-vivo or in-vitro studies. Results: In the rat renal unilateral clamping model, pretreatment with PD128907 (0.2 mg/kg, IV) protected against renal I/R injury and increased survival rate during a long-term follow-up after seven days. A decrease in the generation of ROS, apoptosis and inflammation may be involved in the D3R-mediated protection since pretreatment with PD128907 increased renal glutathione and superoxide dismutase levels and decreased malondialdehyde levels in the I/R group. The increase in cytokines (TNF-?, IL-1?, and IL-10) and myeloperoxidase in I/R injured kidney was also prevented with a , simultaneous decrease in the apoptosis of the epithelial cells and expression of apoptosis biomarkers in kidney harvested one day after I/R injury. The increase in the co-immunoprecipitation between D3R and G?12 with D3R stimulation paralleled the observed renal protection from I/R injury. Moreover, in vitro studies showed that transient overexpression of G?12 in the NRK52E cells attenuated the protective effect of PD128907 on H/R injury. The protective effect of PD128907 might be of significance to renal transplantation, since cold storage/rewarming induced injury increased LDH release and decreased cell viability in NRK52E cells. Conversely, in the presence of PD128907, the increased LDH release and decreased cell viability were reversed. Conclusion: These results suggest that activation of D3R, by decreasing G?12-induced renal damage, may exert a protective effect from I/R injury. äStimulation of Dopamine D3 Receptor Attenuates Renal Ischemia/Reperfus(epmc).pdf DeepDyve Pubget Overpricing