Up-regulation of miR-26a promotes apoptosis of hypoxic rat neonatal cardiomyocytes by repressing GSK-3β protein expression

Suh, Jong Hui; Choi, Eunmi; Cha, Min‐Ji; Song, Bomi; Ham, Ok Kyung; Lee, Seyeon; Yoon, Cheesoon; Lee, Changyeon; Park, Jun‐Hee; Lee, Sun Hee; Hwang, Ki‐Chul

doi:10.1016/j.bbrc.2012.05.138

Cited by 55 publications

(46 citation statements)

References 36 publications

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“…In addition, miR-26a overexpression in CM’s decreased GSK3β protein expression suggesting a role for GSK3β in miR-26a-mediated apoptosis in cardiac myocytes. (Suh et al, 2012) These data suggest that neutralization of miR-26a may increase CM cell survival.…”

Section: Mir-26 In Cardiomyocyte Biologymentioning

confidence: 83%

An emerging role for the miR-26 family in cardiovascular disease

Icli

Dorbala

Feinberg

2014

Trends in Cardiovascular Medicine

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In response to acute myocardial infarction (MI), a complex series of cellular and molecular signaling events orchestrate the myocardial remodeling that ensues weeks to months after injury. Clinical, epidemiological, and pathological studies demonstrate that inadequate or impaired angiogenesis after myocardial injury is often associated with decreased left ventricular (LV) function and clinical outcomes. The microRNA family, miR-26, plays diverse roles in regulating key aspects of cellular growth, development, and activation. Recent evidence supports a central role for the miR-26 family in cardiovascular disease by controlling critical signaling pathways, such as BMP/SMAD1 signaling, and targets relevant to endothelial cell growth, angiogenesis, and LV function post-MI. Emerging studies of the miR-26 family in other cell types including vascular smooth muscle cells, cardiac fibroblasts, and cardiomyocytes suggest that miR-26 may bear important implications for a range of cardiovascular repair mechanisms. This review examines the current knowledge of the miR-26 family’s role in key cell types that critically control cardiovascular disease under pathological and physiological stimuli

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Section: Mir-26 In Cardiomyocyte Biologymentioning

confidence: 83%

An emerging role for the miR-26 family in cardiovascular disease

Icli

Dorbala

Feinberg

2014

Trends in Cardiovascular Medicine

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“…In different types of cancers, miR-26a has been reported to be either up-regulated or down-regulated, and exhibits either an oncogenic or a tumor-suppressor function [62–68], suggesting the expressional regulation and pathological function of miR-26a are cell context dependent. A set of target genes of miR-26a, such as HGMA1 [62], EZH2 [63], MCL-1 [64], FGF9 [65] and GSK-GSK - 3β [67], have been reported previously.…”

Section: Discussionmentioning

confidence: 99%

Identification of MLL-fusion/MYC⊣miR-26⊣TET1 signaling circuit in MLL-rearranged leukemia

et al. 2016

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Expression of functionally important genes is often tightly regulated at both transcriptional and post-transcriptional levels. We reported previously that TET1, the founding member of the TET methylcytosine dioxygenase family, plays an essential oncogenic role in MLL-rearranged acute myeloid leukemia (AML) where it is overexpressed owing to MLL-fusion-mediated direct up-regulation at the transcriptional level. Here we show that the overexpression of TET1 in MLL-rearranged AML also relies on the down-regulation of miR-26a, which directly negatively regulates TET1 expression at the post-transcriptional level. Through inhibiting expression of TET1 and its downstream targets, forced expression of miR-26a significantly suppresses the growth/viability of human MLL-rearranged AML cells, and substantially inhibits MLL-fusion-mediated mouse hematopoietic cell transformation and leukemogenesis. Moreover, c-Myc, an oncogenic transcription factor up-regulated in MLL-rearranged AML, mediates the suppression of miR-26a expression at the transcriptional level. Collectively, our data reveal a previously unappreciated signaling pathway involving the MLL-fusion/MYC⊣miR-26a⊣TET1 signaling circuit, in which miR-26a functions as an essential tumor-suppressor mediator and its transcriptional repression is required for the overexpression and oncogenic function of TET1 in MLL-rearranged AML. Thus, restoration of miR-26a expression/function holds therapeutic potential to treat MLL-rearranged AML.

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“…Moreover, miRNAs are also involved in the regulation of apoptosis. Up-regulation of miR-26a promotes apoptosis in rat neonatal cardiomyocytes via the caspase-3 pathway [42] while down-regulation of miR-26a antagonizes apoptosis by targeting MTDH and EZH2 in breast cancer [43]. Let-7 is also a regulator of apoptosis in tumors [44].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA and mRNA expression profiling in rat acute respiratory distress syndrome

Huang

Xiao²,

Chintagari³

et al. 2014

BMC Med Genomics

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BackgroundAcute respiratory distress syndrome (ARDS) is characterized by pulmonary epithelial injury and extensive inflammation of the pulmonary parenchyma. Systematic analyses of microRNA (miRNA) and mRNA expression profiling in ARDS provide insights into understanding of molecular mechanisms of the pathogenesis of ARDS. The objective of this study was to identify miRNA and mRNA interactions in a rat model of ARDS by combining miRNA and mRNA microarray analyses.MethodsRat model of ARDS was induced by saline lavage and mechanical ventilation. The expression profiles of both mRNAs and miRNAs in rat ARDS model were performed by microarray analyses. Microarray data were further verified by quantitative RT-PCR. Functional annotation on dys-regulated mRNAs and miRNAs was carried out by bioinformatics analysis.ResultsThe expression of 27 miRNAs and 37 mRNAs were found to be significantly changed. The selected miRNAs and genes were further verified by quantitative real-time PCR. The down-regulated miRNAs included miR-24, miR-26a, miR-126, and Let-7a, b, c, f. The up-regulated miRNAs were composed of miR-344, miR-346, miR-99a, miR-127, miR-128b, miR-135b, and miR-30a/b. Gene ontology and functional annotation analyses indicated that up-regulated mRNAs, such as Apc, Timp1, and Sod2, were involved in the regulation of apoptosis. Bioinformatics analysis showed the inverse correlation of altered miRNAs with the expression of their predicted target mRNAs. While Sod2 was inversely correlated with Let-7a, b, c, f., Ebf1 and Apc were inversely correlated with miR-24 and miR-26a, respectively. miR-26a, miR-346, miR-135b, miR-30a/b, miR-344, and miR-18a targeted multiple altered mRNAs. Gabrb1, Sod2, Eif2ak1, Fbln5, and Tspan8 were targeted by multiple altered miRNAs.ConclusionThe expressions of miRNAs and mRNAs were altered in a rat model of ARDS. The identified miRNA-mRNA pairs may play critical roles in the pathogenesis of ARDS.

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Up-regulation of miR-26a promotes apoptosis of hypoxic rat neonatal cardiomyocytes by repressing GSK-3β protein expression

Cited by 55 publications

References 36 publications

An emerging role for the miR-26 family in cardiovascular disease

An emerging role for the miR-26 family in cardiovascular disease

Identification of MLL-fusion/MYC⊣miR-26⊣TET1 signaling circuit in MLL-rearranged leukemia

MicroRNA and mRNA expression profiling in rat acute respiratory distress syndrome

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