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10.1371/journal.pone.0174108 http://scihub22266oqcxt.onion/10.1371/journal.pone.0174108 C5360327!5360327!28323879     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 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 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       PLoS+One 2017 ; 12 (3): ä Nephropedia Template TP {{tp|p=28323879|t=2017. miR-181b regulates vascular stiffness age dependently in part by regulating TGF-? signaling |pdf=|usr=}}{{28323879}} gab.com Text miR-181b regulates vascular stiffness age dependently in part by regulating TGF- signaling JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=28323879 #FOAvip Background: Endothelial dysfunction and arterial stiffening play major roles in cardiovascular diseases. The critical role for the miR-181 family in vascular inflammation has been documented. Here we tested whether the miR-181 family can influence the pathogenesis of hypertension and vascular stiffening. Methods and results: qPCR data showed a significant decrease in miR-181b expression in the aorta of the older mice. Eight miR-181a1/b1-/- mice and wild types (C57BL6J:WT) were followed weekly for pulse wave velocity (PWV) and blood pressure measurements. After 20 weeks, the mice were tested for endothelial function and aortic modulus. There was a progressive increase in PWV and higher systolic blood pressure in miR-181a1/b1-/- mice compared with WTs. At 21 weeks, aortic modulus was significantly greater in the miR-181a1/b1-/- group, and serum TGF-? was found to be elevated at this time. A luciferase reporter assay confirmed miR-181b targets TGF-?i (TGF-? induced) in the aortic VSMCs. In contrast, wire myography revealed unaltered endothelial function along with higher nitric oxide production in the miR-181a1/b1-/- group. Cultured VECs and VSMCs from the mouse aorta showed more secreted TGF-? in VSMCs of the miR-181a1/b1-/- group; whereas, no change was observed from VECs. Circulating levels of angiotensin II were similar in both groups. Treatment with losartan (0.6 g/L) prevented the increase in PWV, blood pressure, and vascular stiffness in miR-181a1/b1-/- mice. Immunohistochemistry and western blot for p-SMAD2/3 validated the inhibitory effect of losartan on TGF-? signaling in miR-181a1/b1-/- mice. Conclusions: Decreased miR-181b with aging plays a critical role in ECM remodeling by removing the brake on the TGF-?, pSMAD2/3 pathway. Twit Text FOAVip miR-181b regulates vascular stiffness age dependently in part by regulating TGF- signaling ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=28323879 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28323879 #FOAvip English Wikipedia <ref>{{Cite pmid|28323879}}</ref> miR-181b regulates vascular stiffness age dependently in part by regulating TGF-? signaling #MMPMID28323879 Hori D; Dunkerly-Eyring B; Nomura Y; Biswas D; Steppan J; Henao-Mejia J; Adachi H; Santhanam L; Berkowitz DE; Steenbergen C; Flavell RA; Das S PLoS One 2017[]; 12 (3): ä PMID28323879show ga Background: Endothelial dysfunction and arterial stiffening play major roles in cardiovascular diseases. The critical role for the miR-181 family in vascular inflammation has been documented. Here we tested whether the miR-181 family can influence the pathogenesis of hypertension and vascular stiffening. Methods and results: qPCR data showed a significant decrease in miR-181b expression in the aorta of the older mice. Eight miR-181a1/b1-/- mice and wild types (C57BL6J:WT) were followed weekly for pulse wave velocity (PWV) and blood pressure measurements. After 20 weeks, the mice were tested for endothelial function and aortic modulus. There was a progressive increase in PWV and higher systolic blood pressure in miR-181a1/b1-/- mice compared with WTs. At 21 weeks, aortic modulus was significantly greater in the miR-181a1/b1-/- group, and serum TGF-? was found to be elevated at this time. A luciferase reporter assay confirmed miR-181b targets TGF-?i (TGF-? induced) in the aortic VSMCs. In contrast, wire myography revealed unaltered endothelial function along with higher nitric oxide production in the miR-181a1/b1-/- group. Cultured VECs and VSMCs from the mouse aorta showed more secreted TGF-? in VSMCs of the miR-181a1/b1-/- group; whereas, no change was observed from VECs. Circulating levels of angiotensin II were similar in both groups. Treatment with losartan (0.6 g/L) prevented the increase in PWV, blood pressure, and vascular stiffness in miR-181a1/b1-/- mice. Immunohistochemistry and western blot for p-SMAD2/3 validated the inhibitory effect of losartan on TGF-? signaling in miR-181a1/b1-/- mice. Conclusions: Decreased miR-181b with aging plays a critical role in ECM remodeling by removing the brake on the TGF-?, pSMAD2/3 pathway. ämiR-181b regulates vascular stiffness age dependently in part by regul(epmc).pdf DeepDyve Pubget Overpricing