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10.1161/STROKEAHA.115.010567 http://scihub22266oqcxt.onion/10.1161/STROKEAHA.115.010567 C4624519!4624519 !26451018     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26451018 &cmd=llinks): Failed to open stream: HTTP request failed! 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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 proliferation. We aimed to determine whether the expression of 3 miRNAs that regulate vascular smooth muscle cell proliferation (miR-145, miR-221, and miR-222) is 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 3 distinct clinical scenarios: (1) patients without previous neurological events but high-grade carotid stenosis (asymptomatic), (2) patients with an acute neurological event within 5 days of the CEA (urgent), and (3) patients undergoing CEA>5 days after a neurological 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, whereas no significant differences were seen in miR-145 across the 3 groups. Regression analysis demonstrated a significant correlation between time from the neurological event to CEA and increasing miR-221 and miR-222, but not miR-145. mRNA encoding p27Kip1, a target of miR-221 and miR-222 that inhibits vascular smooth muscle cell proliferation, was increased in the urgent group. CONCLUSIONS: Atherosclerotic plaque rupture is accompanied by a loss of miR-221 and miR-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 Jr ; Woods TC Stroke 2015[Nov]; 46 (11 ): 3285-7 PMID26451018 show 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 proliferation. We aimed to determine whether the expression of 3 miRNAs that regulate vascular smooth muscle cell proliferation (miR-145, miR-221, and miR-222) is 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 3 distinct clinical scenarios: (1) patients without previous neurological events but high-grade carotid stenosis (asymptomatic), (2) patients with an acute neurological event within 5 days of the CEA (urgent), and (3) patients undergoing CEA>5 days after a neurological 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, whereas no significant differences were seen in miR-145 across the 3 groups. Regression analysis demonstrated a significant correlation between time from the neurological event to CEA and increasing miR-221 and miR-222, but not miR-145. mRNA encoding p27Kip1, a target of miR-221 and miR-222 that inhibits vascular smooth muscle cell proliferation, was increased in the urgent group. CONCLUSIONS: Atherosclerotic plaque rupture is accompanied by a loss of miR-221 and miR-222 and an increase in p27Kip1 mRNA expression in the plaque shoulder, suggesting an association between these miRNAs and atherosclerotic plaque stability. |*Asymptomatic Diseases [MESH] |Aged [MESH] |Carotid Stenosis/*genetics/surgery [MESH] |Cyclin-Dependent Kinase Inhibitor p27/genetics [MESH] |Endarterectomy, Carotid [MESH] |Female [MESH] |Gene Expression Profiling [MESH] |Humans [MESH] |Linear Models [MESH] |Male [MESH] |MicroRNAs/genetics [MESH] |Middle Aged [MESH] |Muscle, Smooth, Vascular/metabolism [MESH] |Plaque, Atherosclerotic/*genetics/surgery [MESH] |RNA, Messenger/*metabolism [MESH] |Real-Time Polymerase Chain Reaction [MESH] |Rupture, Spontaneous [MESH] |STAT5 Transcription Factor/genetics [MESH] |Stem Cell Factor/genetics [MESH]Acute Loss of miR-221 and miR-222 in the Atherosclerotic Plaque Should(epmc).pdf DeepDyve Pubget Overpricing