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10.1172/JCI77656 http://scihub22266oqcxt.onion/10.1172/JCI77656 C4362262!4362262!25664856     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Clin+Invest 2015 ; 125 (3): 1228-42 Nephropedia Template TP {{tp|p=25664856|t=2015. EP3 receptor deficiency attenuates pulmonary hypertension through suppression of Rho/TGF-?1 signaling |pdf=|usr=}}{{25664856}} gab.com Text EP3 receptor deficiency attenuates pulmonary hypertension through suppression of Rho/TGF- 1 signaling JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=25664856 #FOAvip Pulmonary arterial hypertension (PAH) is commonly associated with chronic hypoxemia in disorders such as chronic obstructive pulmonary disease (COPD). Prostacyclin analogs are widely used in the management of PAH patients; however, clinical efficacy and long-term tolerability of some prostacyclin analogs may be compromised by concomitant activation of the E-prostanoid 3 (EP3) receptor. Here, we found that EP3 expression is upregulated in pulmonary arterial smooth muscle cells (PASMCs) and human distal pulmonary arteries (PAs) in response to hypoxia. Either pharmacological inhibition of EP3 or Ep3 deletion attenuated both hypoxia and monocrotaline-induced pulmonary hypertension and restrained extracellular matrix accumulation in PAs in rodent models. In a murine PAH model, Ep3 deletion in SMCs, but not endothelial cells, retarded PA medial thickness. Knockdown of EP3? and EP3?, but not EP3?, isoforms diminished hypoxia-induced TGF-?1 activation. Expression of either EP3? or EP3? in EP3-deficient PASMCs restored TGF-?1 activation in response to hypoxia. EP3?/? activation in PASMCs increased RhoA-dependent membrane type 1 extracellular matrix metalloproteinase (MMP) translocation to the cell surface, subsequently activating pro?MMP-2 and promoting TGF-?1 signaling. Activation or disruption of EP3 did not influence PASMC proliferation. Together, our results indicate that EP3 activation facilitates hypoxia-induced vascular remodeling and pulmonary hypertension in mice and suggest EP3 inhibition as a potential therapeutic strategy for pulmonary hypertension. Twit Text FOAVip EP3 receptor deficiency attenuates pulmonary hypertension through suppression of Rho/TGF- 1 signaling ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=25664856 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25664856 #FOAvip English Wikipedia <ref>{{Cite pmid|25664856}}</ref> EP3 receptor deficiency attenuates pulmonary hypertension through suppression of Rho/TGF-?1 signaling #MMPMID25664856 Lu A; Zuo C; He Y; Chen G; Piao L; Zhang J; Xiao B; Shen Y; Tang J; Kong D; Alberti S; Chen D; Zuo S; Zhang Q; Yan S; Fei X; Yuan F; Zhou B; Duan S; Yu Y; Lazarus M; Su Y; Breyer RM; Funk CD; Yu Y J Clin Invest 2015[Mar]; 125 (3): 1228-42 PMID25664856show ga Pulmonary arterial hypertension (PAH) is commonly associated with chronic hypoxemia in disorders such as chronic obstructive pulmonary disease (COPD). Prostacyclin analogs are widely used in the management of PAH patients; however, clinical efficacy and long-term tolerability of some prostacyclin analogs may be compromised by concomitant activation of the E-prostanoid 3 (EP3) receptor. Here, we found that EP3 expression is upregulated in pulmonary arterial smooth muscle cells (PASMCs) and human distal pulmonary arteries (PAs) in response to hypoxia. Either pharmacological inhibition of EP3 or Ep3 deletion attenuated both hypoxia and monocrotaline-induced pulmonary hypertension and restrained extracellular matrix accumulation in PAs in rodent models. In a murine PAH model, Ep3 deletion in SMCs, but not endothelial cells, retarded PA medial thickness. Knockdown of EP3? and EP3?, but not EP3?, isoforms diminished hypoxia-induced TGF-?1 activation. Expression of either EP3? or EP3? in EP3-deficient PASMCs restored TGF-?1 activation in response to hypoxia. EP3?/? activation in PASMCs increased RhoA-dependent membrane type 1 extracellular matrix metalloproteinase (MMP) translocation to the cell surface, subsequently activating pro?MMP-2 and promoting TGF-?1 signaling. Activation or disruption of EP3 did not influence PASMC proliferation. Together, our results indicate that EP3 activation facilitates hypoxia-induced vascular remodeling and pulmonary hypertension in mice and suggest EP3 inhibition as a potential therapeutic strategy for pulmonary hypertension. äEP3 receptor deficiency attenuates pulmonary hypertension through supp(epmc).pdf DeepDyve Pubget Overpricing