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10.1161/STROKEAHA.115.010567 http://scihub22266oqcxt.onion/10.1161/STROKEAHA.115.010567 C4624519!4624519!26451018     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Stroke 2015 ; 46 (11): 3285-7 Nephropedia Template TP {{tp|p=26451018|t=2015. Acute loss of miR-221 and miR-222 in the atherosclerotic plaque shoulder accompanies plaque rupture |pdf=|usr=}}{{26451018}} gab.com Text Acute loss of miR-221 and miR-222 in the atherosclerotic plaque shoulder accompanies plaque rupture JO: Stroke http://www.kidney.de/pget.php?&tw=1&pmid=26451018 #FOAvip Background and Purpose: Atherosclerotic plaque vulnerability is accompanied by changes in the molecular and cellular function in the plaque shoulder, including a decrease in vascular smooth muscle cell (VSMC) proliferation. We aimed to determine if the expression of three miRNAs that regulate VSMC proliferation (miR-145, miR-221, and miR-222) are altered with plaque rupture, suggesting a role in regulating plaque stability. Methods: miRNAs were measured in the plaque shoulder of carotid plaques obtained from patients undergoing carotid endarterectomy (CEA) for three distinct clinical scenarios: 1) patients without prior neurologic events but high-grade carotid stenosis (asymptomatic), 2) patients with an acute neurologic event within 5 days of the CEA (urgent), and 3) patients undergoing CEA > 5 days after a neurologic event (symptomatic). Results: Mean time from plaque rupture event to CEA was 2.4 days in the urgent group. The urgent group exhibited a significant decrease in miR-221 and miR-222 expression in the plaque shoulder while no significant differences were seen in miR-145 across the three groups. Regression analysis demonstrated a significant correlation between time from the neurologic event to CEA and increasing miR-221 and miR-222, but not miR-145. mRNA encoding p27Kip1, a target of miR-221 and -222 that inhibits VSMC proliferation, was increased in the urgent group. Conclusions: Atherosclerotic plaque rupture is accompanied by a loss of miR-221 and -222 and an increase in p27Kip1 mRNA expression in the plaque shoulder, suggesting an association between these miRNAs and atherosclerotic plaque stability. Twit Text FOAVip Acute loss of miR-221 and miR-222 in the atherosclerotic plaque shoulder accompanies plaque rupture ????Stroke http://www.kidney.de/pget.php?&tw=1&pmid=26451018 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26451018 #FOAvip English Wikipedia <ref>{{Cite pmid|26451018}}</ref> Acute loss of miR-221 and miR-222 in the atherosclerotic plaque shoulder accompanies plaque rupture #MMPMID26451018 Bazan HA; Hatfield SA; O'Malley CB; Brooks AJ; Lightell D; Woods TC Stroke 2015[Nov]; 46 (11): 3285-7 PMID26451018show ga Background and Purpose: Atherosclerotic plaque vulnerability is accompanied by changes in the molecular and cellular function in the plaque shoulder, including a decrease in vascular smooth muscle cell (VSMC) proliferation. We aimed to determine if the expression of three miRNAs that regulate VSMC proliferation (miR-145, miR-221, and miR-222) are altered with plaque rupture, suggesting a role in regulating plaque stability. Methods: miRNAs were measured in the plaque shoulder of carotid plaques obtained from patients undergoing carotid endarterectomy (CEA) for three distinct clinical scenarios: 1) patients without prior neurologic events but high-grade carotid stenosis (asymptomatic), 2) patients with an acute neurologic event within 5 days of the CEA (urgent), and 3) patients undergoing CEA > 5 days after a neurologic event (symptomatic). Results: Mean time from plaque rupture event to CEA was 2.4 days in the urgent group. The urgent group exhibited a significant decrease in miR-221 and miR-222 expression in the plaque shoulder while no significant differences were seen in miR-145 across the three groups. Regression analysis demonstrated a significant correlation between time from the neurologic event to CEA and increasing miR-221 and miR-222, but not miR-145. mRNA encoding p27Kip1, a target of miR-221 and -222 that inhibits VSMC proliferation, was increased in the urgent group. Conclusions: Atherosclerotic plaque rupture is accompanied by a loss of miR-221 and -222 and an increase in p27Kip1 mRNA expression in the plaque shoulder, suggesting an association between these miRNAs and atherosclerotic plaque stability. äAcute loss of miR-221 and miR-222 in the atherosclerotic plaque should(epmc).pdf DeepDyve Pubget Overpricing