2011
DOI: 10.1084/jem.20101812
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Role for miR-204 in human pulmonary arterial hypertension

Abstract: Reduced miR-204 expression facilitates the excessive proliferation and apoptosis resistance of pulmonary artery smooth muscle cells characteristic of human pulmonary arterial hypertension.

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Cited by 471 publications
(357 citation statements)
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References 66 publications
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“…The following interventions were performed on the animals: Rats with established PAH (3 weeks after monocrotaline injection) were randomized to receive no treatment, 6 μg of in vivo-ready miR-126-5p mimic (Life Technologies, Burlington, ON, Canada), or miR-control (Life Technologies) prepared as previously described 18 and injected intravenously every 48 hours for 2 weeks. In a fourth treatment, to evaluate the tissue distribution, 6 μg fluorescent in vivo-ready miR-126-5p (Alexa Fluor 647-labeled in vivo-ready miR-126-5p mimic, Life Technologies) was injected intravenously every 48 hours for 2 weeks.…”
Section: Animal Modelmentioning
confidence: 99%
See 1 more Smart Citation
“…The following interventions were performed on the animals: Rats with established PAH (3 weeks after monocrotaline injection) were randomized to receive no treatment, 6 μg of in vivo-ready miR-126-5p mimic (Life Technologies, Burlington, ON, Canada), or miR-control (Life Technologies) prepared as previously described 18 and injected intravenously every 48 hours for 2 weeks. In a fourth treatment, to evaluate the tissue distribution, 6 μg fluorescent in vivo-ready miR-126-5p (Alexa Fluor 647-labeled in vivo-ready miR-126-5p mimic, Life Technologies) was injected intravenously every 48 hours for 2 weeks.…”
Section: Animal Modelmentioning
confidence: 99%
“…At that point, TAPSE and the S wave were slightly decreased, but stroke volume, cardiac output, and RV end-diastolic pressure were unchanged (CRVH stage). By the third to fourth week, the RV size was increased, along with RV end-diastolic pressure, whereas TAPSE, S wave, stroke volume, and cardiac output were significantly decreased, and obvious signs of heart failure (ie, ascites) and morbidity (ie, weight loss) were observable in the rats (DRV stage).The following interventions were performed on the animals: Rats with established PAH (3 weeks after monocrotaline injection) were randomized to receive no treatment, 6 μg of in vivo-ready miR-126-5p mimic (Life Technologies, Burlington, ON, Canada), or miR-control (Life Technologies) prepared as previously described 18 and injected intravenously every 48 hours for 2 weeks. In a fourth treatment, to evaluate the tissue distribution, 6 μg fluorescent in vivo-ready miR-126-5p (Alexa Fluor 647-labeled in vivo-ready miR-126-5p mimic, Life Technologies) was injected intravenously every 48 hours for 2 weeks.…”
mentioning
confidence: 99%
“…We and others have described the implication of the receptor of advanced glycation endproducts, 2-4 the oncoprotein kinase Pim-1 3,5 and the transcription factor nuclear factor of activated T cells 6,7 in promoting proliferation in remodeling processes occurring in both VRD and PAH. In PAH patients' lung vasculature, these molecular actors are, at least in part, regulated by proinflammatory cytokines, alterations in the miR-223/DNA damage/ Poly[ADP-ribose] polymerase 1/miR-204 axis [8][9][10][11] and subsequent overexpression of the epigenetic reader bromodomain protein 4 (BRD4). 12 BRD4 functions as a scaffold for transcription factors at promoters and superenhancers, modulating the chromatin landscape and facilitating transcriptional activation of target genes.…”
Section: P Ulmonary Arterial Hypertension (Pah) Is a Vascularmentioning
confidence: 99%
“…9,10 This results in the proproliferative and antiapoptotic phenotype of PAH pulmonary artery smooth muscle cells (PASMCs). …”
mentioning
confidence: 99%