miR-24 inhibits apoptosis and represses Bim in mouse cardiomyocytes

Li, Qian; Laake, Linda W. van; Huang, Yu; Liu, Siyuan; Wendland, Michael F.; Srivastava, Deepak

doi:10.1084/jem.20101547

Cited by 285 publications

(268 citation statements)

References 43 publications

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“…Mammalian BH3-only genes are also subject to post-transcriptional regulation via microRNAs (miRNAs). It has been demonstrated, for example, that the 3 ′ untranslated region (UTR) of Bim mRNA is the target of several miRNAs, which act to down-regulate and fine-tune Bim expression (Ventura et al 2008;Kole et al 2011;Qian et al 2011;Pernaute et al 2014; for review, see Sionov et al 2015).…”

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confidence: 99%

miRNAs cooperate in apoptosis regulation during C. elegans development

et al. 2017

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Programmed cell death occurs in a highly reproducible manner during Caenorhabditis elegans development. We demonstrate that, during embryogenesis, miR-35 and miR-58 bantam family microRNAs (miRNAs) cooperate to prevent the precocious death of mothers of cells programmed to die by repressing the gene egl-1, which encodes a proapoptotic BH3-only protein. In addition, we present evidence that repression of egl-1 is dependent on binding sites for miR-35 and miR-58 family miRNAs within the egl-1 3 ′ untranslated region (UTR), which affect both mRNA copy number and translation. Furthermore, using single-molecule RNA fluorescent in situ hybridization (smRNA FISH), we show that egl-1 is transcribed in the mother of a cell programmed to die and that miR-35 and miR-58 family miRNAs prevent this mother from dying by keeping the copy number of egl-1 mRNA below a critical threshold. Finally, miR-35 and miR-58 family miRNAs can also dampen the transcriptional boost of egl-1 that occurs specifically in a daughter cell that is programmed to die. We propose that miRNAs compensate for lineagespecific differences in egl-1 transcriptional activation, thus ensuring that EGL-1 activity reaches the threshold necessary to trigger death only in daughter cells that are programmed to die.

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confidence: 99%

miRNAs cooperate in apoptosis regulation during C. elegans development

et al. 2017

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“…(5) In addition, several studies indicated a crucial role for miRNA -dependent regulation of cardiac angiogenesis, fibrosis, and cardiomyocyte hypertrophy upon MI. (101,105,128,129) These observations clearly link cardiac ischemic disease to altered miR expression. However, miRNA deregulation also offers a new therapeutic entry point to counteract MI-induced cardiac dysfunction.…”

Section: Mirnas In Glucose Homeostasismentioning

confidence: 79%

MicroRNAs in Cardiometabolic Diseases

Meiliana

Wijaya

2013

Indones Biomed J

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BACKGROUND: MicroRNAs (miRNAs) are ~22-nucleotide noncoding RNAs with critical functions in multiple physiological and pathological processes. An explosion of reports on the discovery and characterization of different miRNA species and their involvement in almost every aspect of cardiac biology and diseases has established an exciting new dimension in gene regulation networks for cardiac development and pathogenesis.CONTENT: Alterations in the metabolic control of lipid and glucose homeostasis predispose an individual to develop cardiometabolic diseases, such as type 2 diabetes mellitus and atherosclerosis. Work over the last years has suggested that miRNAs play an important role in regulating these physiological processes. Besides a cell-specific transcription factor profile, cell-specific miRNA-regulated gene expression is integral to cell fate and activation decisions. Thus, the cell types involved in atherosclerosis, vascular disease, and its myocardial sequelae may be differentially regulated by distinct miRNAs, thereby controlling highly complex processes, for example, smooth muscle cell phenotype and inflammatory responses of endothelial cells or macrophages. The recent advancements in using miRNAs as circulating biomarkers or therapeutic modalities, will hopefully be able to provide a strong basis for future research to further expand our insights into miRNA function in cardiovascular biology. ISI:Perubahan kendali metabolisme lemak dan homeostasis glukosa pada individu dapat memicu berkembangnya penyakit kardiometabolik seperti diabetes melitus tipe 2 dan aterosklerosis. Penelitian yang dilakukan pada dasawarsa terakhir telah menunjukkan bahwa miRNA memiliki peran penting dalam pengaturan proses fisiologi ini. Selain profil faktor transkripsi spesifik sel, ekspresi gen yang diregulasi oleh miRNA mempengaruhi tujuan akhir perkembangan dan keputusan aktivasi sel. Jadi, tipe sel yang terlibat dalam aterosklerosis, penyakit vaskular, dan kerusakan miokardial mungkin diregulasi secara berbeda oleh miRNA yang berlainan, melalui proses pengaturan yang sangat rumit, misalnya fenotipe sel otot polos dan respon inflamasi sel endotel atau makrofag. Perkembangan terakhir dalam hal penggunaan miRNA sebagai biomarker atau modalitas terapi diharapkan dapat menjadi dasar yang kuat untuk penelitian lebih lanjut, sehingga dapat memperkaya pemahaman kita mengenai fungsi miRNA pada biologi kardiovaskular. RINGKASAN:MiRNA adalah noncoding RNA yang kecil, berfungsi sebagai pengatur post-transkripsi pada ekspresi gen. MiRNA merupakan modulator potensial pada berbagai proses dan patologi biologi. Penemuan yang ada menunjukkan pentingnya peran miRNA pada vaskulatur, alur metabolisme lemak, dan homeostasis glukosa. Abstract Abstrak R E V I E W A R T I C L E

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“…Since it has been reported that SIRT1 was upregulated, leading to deacetylation and inactivation of HIF-1α in hypoxia [47], it would be interesting to examine the crosstalk between miR-199/SIRT1/HIF1a. Recently, the Srivastava Deepark lab reported that miRNA-24 expression is downregulated in the ischemic border zone of the murine left ventricle following MI [48]. miR-24 suppresses cardiomyocyte apoptosis, in part by direct repression of Bim, the BH3-only domain-containing protein, which positively regulates apoptosis.…”

Section: Ischemic Cardiomyopathymentioning

confidence: 99%

Cardinal roles of miRNA in cardiac development and disease

Feng

2011

Sci. China Life Sci.

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MicroRNAs (miRNAs) are small noncoding RNAs that are emerging as pivotal modulators in virtually all aspects of cardiac biology, from cardiac development to cardiomyocyte survival and hypertrophy. The miRNA profiling, following gain-and loss-of-function studies using in vitro and in vivo models, has identified wide-ranging functions for miRNAs in the heart, providing new perspectives on their contributions to cardiac pathogenesis, and revealing potential therapeutic targets and diagnostic biomarkers. This review summarizes current progress in regulation of miRNAs in heart development and disease. miRNA, cardiac, development, disease Citation:Feng Y L, Yu X Y. Cardinal roles of miRNA in cardiac development and disease.

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miR-24 inhibits apoptosis and represses Bim in mouse cardiomyocytes

Abstract: In part by repressing expression of Bim, microRNA-24 reduces cardiomyocyte loss in a mouse model of myocardial infarction.

Cited by 285 publications

References 43 publications

miRNAs cooperate in apoptosis regulation during C. elegans development

miRNAs cooperate in apoptosis regulation during C. elegans development

MicroRNAs in Cardiometabolic Diseases

Cardinal roles of miRNA in cardiac development and disease

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