Journal articles: 'MicroRNA turnover'

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Sanei, Maryam, and Xuemei Chen. "Mechanisms of microRNA turnover." Current Opinion in Plant Biology 27 (October 2015): 199–206. http://dx.doi.org/10.1016/j.pbi.2015.07.008.

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Michaud, Pascale, Vivek Nilesh Shah, Pauline Adjibade, Francois Houle, Miguel Quévillon Huberdeau, Rachel Rioux, Camille Lavoie-Ouellet, Weifeng Gu, Rachid Mazroui, and Martin J. Simard. "The RabGAP TBC-11 controls Argonaute localization for proper microRNA function in C. elegans." PLOS Genetics 17, no. 4 (April 7, 2021): e1009511. http://dx.doi.org/10.1371/journal.pgen.1009511.

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Once loaded onto Argonaute proteins, microRNAs form a silencing complex called miRISC that targets mostly the 3’UTR of mRNAs to silence their translation. How microRNAs are transported to and from their target mRNA remains poorly characterized. While some reports linked intracellular trafficking to microRNA activity, it is still unclear how these pathways coordinate for proper microRNA-mediated gene silencing and turnover. Through a forward genetic screen usingCaenorhabditis elegans, we identified the RabGAPtbc-11as an important factor for the microRNA pathway. We show that TBC-11 acts mainly through the small GTPase RAB-6 and that its regulation is required for microRNA function. The absence of functional TBC-11 increases the pool of microRNA-unloaded Argonaute ALG-1 that is likely associated to endomembranes. Furthermore, in this condition, this pool of Argonaute accumulates in a perinuclear region and forms a high molecular weight complex. Altogether, our data suggest that the alteration of TBC-11 generates a fraction of ALG-1 that cannot bind to target mRNAs, leading to defective gene repression. Our results establish the importance of intracellular trafficking for microRNA function and demonstrate the involvement of a small GTPase and its GAP in proper Argonaute localizationin vivo.

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Rogers, K., and X. Chen. "microRNA Biogenesis and Turnover in Plants." Cold Spring Harbor Symposia on Quantitative Biology 77 (January 1, 2012): 183–94. http://dx.doi.org/10.1101/sqb.2013.77.014530.

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Rüegger, Stefan, and Helge Großhans. "MicroRNA turnover: when, how, and why." Trends in Biochemical Sciences 37, no. 10 (October 2012): 436–46. http://dx.doi.org/10.1016/j.tibs.2012.07.002.

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Zhang, Zhuo, Yong-Wen Qin, Gary Brewer, and Qing Jing. "MicroRNA degradation and turnover: regulating the regulators." Wiley Interdisciplinary Reviews: RNA 3, no. 4 (March 28, 2012): 593–600. http://dx.doi.org/10.1002/wrna.1114.

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Medina, Lisvaneth, Jesús Alejandro Guerrero-Muñoz, Ana Isabel Liempi, Christian Castillo, Yessica Ortega, Alfredo Sepúlveda, Fernando Salomó, Juan Diego Maya, and Ulrike Kemmerling. "Ex Vivo Infection of Human Placental Explants by Trypanosoma cruzi Reveals a microRNA Profile Similar to That Seen in Trophoblast Differentiation." Pathogens 11, no. 3 (March 16, 2022): 361. http://dx.doi.org/10.3390/pathogens11030361.

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Congenital Chagas disease, caused by the protozoan parasite Trypanosoma cruzi, is responsible for 22.5% of new cases each year. However, placental transmission occurs in only 5% of infected mothers and it has been proposed that the epithelial turnover of the trophoblast can be considered a local placental defense against the parasite. Thus, Trypanosoma cruzi induces cellular proliferation, differentiation, and apoptotic cell death in the trophoblast, which are regulated, among other mechanisms, by small non-coding RNAs such as microRNAs. On the other hand, ex vivo infection of human placental explants induces a specific microRNA profile that includes microRNAs related to trophoblast differentiation such as miR-512-3p miR-515-5p, codified at the chromosome 19 microRNA cluster. Here we determined the expression validated target genes of miR-512-3p and miR-515-5p, specifically human glial cells missing 1 transcription factor and cellular FLICE-like inhibitory protein, as well as the expression of the main trophoblast differentiation marker human chorionic gonadotrophin during ex vivo infection of human placental explants, and examined how the inhibition or overexpression of both microRNAs affects parasite infection. We conclude that Trypanosoma cruzi-induced trophoblast epithelial turnover, particularly trophoblast differentiation, is at least partially mediated by placenta-specific miR-512-3p and miR-515-5p and that both miRNAs mediate placental susceptibility to ex vivo infection of human placental explants. Knowledge about the role of parasite-modulated microRNAs in the placenta might enable their use as biomarkers, as prognostic and therapeutic tools for congenital Chagas disease in the future.

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Larsson, Erik, Chris Sander, and Debora Marks. "mRNA turnover rate limits siRNA and microRNA efficacy." Molecular Systems Biology 6, no. 1 (January 2010): 454. http://dx.doi.org/10.1038/msb.2010.113.

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Larsson, Erik, Chris Sander, and Debora Marks. "mRNA turnover rate limits siRNA and microRNA efficacy." Molecular Systems Biology 6, no. 1 (January 2010): 433. http://dx.doi.org/10.1038/msb.2010.89.

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Chatterjee, Saibal, and Helge Großhans. "Active turnover modulates mature microRNA activity in Caenorhabditis elegans." Nature 461, no. 7263 (September 2009): 546–49. http://dx.doi.org/10.1038/nature08349.

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Hutvagner, G. "A microRNA in a Multiple-Turnover RNAi Enzyme Complex." Science 297, no. 5589 (August 1, 2002): 2056–60. http://dx.doi.org/10.1126/science.1073827.

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Zlotorynski, Eytan. "Insights into the kinetics of microRNA biogenesis and turnover." Nature Reviews Molecular Cell Biology 20, no. 9 (July 31, 2019): 511. http://dx.doi.org/10.1038/s41580-019-0164-9.

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Gantier, Michael P., Claire E. McCoy, Irina Rusinova, Damien Saulep, Die Wang, Dakang Xu, Aaron T. Irving, et al. "Analysis of microRNA turnover in mammalian cells following Dicer1 ablation." Nucleic Acids Research 39, no. 13 (March 28, 2011): 5692–703. http://dx.doi.org/10.1093/nar/gkr148.

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Li, Yang, Zhixin Li, Shixin Zhou, Jinhua Wen, Bin Geng, Jichun Yang, and Qinghua Cui. "Genome-Wide Analysis of Human MicroRNA Stability." BioMed Research International 2013 (2013): 1–12. http://dx.doi.org/10.1155/2013/368975.

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Increasing studies have shown that microRNA (miRNA) stability plays important roles in physiology. However, the global picture of miRNA stability remains largely unknown. Here, we had analyzed genome-wide miRNA stability across 10 diverse cell types using miRNA arrays. We found that miRNA stability shows high dynamics and diversity both within individual cells and across cell types. Strikingly, we observed a negative correlation between miRNA stability and miRNA expression level, which is different from current findings on other biological molecules such as proteins and mRNAs that show positive and not negative correlations between stability and expression level. This finding indicates that miRNA has a distinct action mode, which we called “rapid production, rapid turnover; slow production, slow turnover.” This mode further suggests that high expression miRNAs normally degrade fast and may endow the cell with special properties that facilitate cellular status-transition. Moreover, we revealed that the stability of miRNAs is affected by cohorts of factors that include miRNA targets, transcription factors, nucleotide content, evolution, associated disease, and environmental factors. Together, our results provided an extensive description of the global landscape, dynamics, and distinct mode of human miRNA stability, which provide help in investigating their functions in physiology and pathophysiology.

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Gutiérrez-Vázquez, Cristina, Anton J. Enright, Ana Rodríguez-Galán, Arantxa Pérez-García, Paul Collier, Matthew R. Jones, Vladimir Benes, et al. "3′ Uridylation controls mature microRNA turnover during CD4 T-cell activation." RNA 23, no. 6 (March 28, 2017): 882–91. http://dx.doi.org/10.1261/rna.060095.116.

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Libri, Valentina, Pascal Miesen, Ronald P. van Rij, and Amy H. Buck. "Regulation of microRNA biogenesis and turnover by animals and their viruses." Cellular and Molecular Life Sciences 70, no. 19 (January 26, 2013): 3525–44. http://dx.doi.org/10.1007/s00018-012-1257-1.

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Jones, Christopher I., and Sarah F. Newbury. "Functions of microRNAs in Drosophila development." Biochemical Society Transactions 38, no. 4 (July 26, 2010): 1137–43. http://dx.doi.org/10.1042/bst0381137.

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Control of mRNA translation and degradation has been shown to be key in the development of complex organisms. The core mRNA degradation machinery is highly conserved in eukaryotes and relies on processive degradation enzymes gaining access to the mRNA. Control of mRNA stability in eukaryotes is also intimately linked to the regulation of translation. A key question in the control of mRNA turnover concerns the mechanisms whereby particular mRNAs are specifically degraded in response to cellular factors. Recently, microRNAs have been shown to bind specifically to mRNAs and regulate their expression via repression of translation and/or degradation. To understand the molecular mechanisms during microRNA repression of mRNAs, it is necessary to identify their biologically relevant targets. However, computational methods have so far proved unreliable, therefore verification of biologically important targets at present requires experimental analysis. The present review aims to outline the mechanisms of mRNA degradation and then focus on the role of microRNAs as factors affecting particular Drosophila developmental processes via their post-transcriptional effects on mRNA degradation and translation. Examples of experimentally verified targets of microRNAs in Drosophila are summarized.

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Mielnik, Jakub, Elżbieta Świętochowska, and Zofia Ostrowska. "Sclerostin, periostin and microRNA as potential markers of osteoporosis." Postępy Higieny i Medycyny Doświadczalnej 73 (March 13, 2019): 133–40. http://dx.doi.org/10.5604/01.3001.0013.0924.

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In recent years, people have had high hopes for the possibility of using measurements of the so-called modern bone turnover markers in diagnosis, diagnostics of the course and the prediction of the occurrence of complications of bone metabolic diseases, especially osteoporosis. So far, several diagnostic markers of bone turnover have been identified, particular importance attached to PINP and CTx. However, many studies have highlighted that their use in the diagnosis of osteoporosis is rather limited due to their inter-individual and intra-individual variability, tissue non-specificity, the inability to evaluate individual bone tissue compartments, and the ability to assess metabolic activity of only osteoblasts and/or osteoclasts without osteocytes. The data presented in the thesis indicates the potential usefulness of sclerostin measurements, primarily associated with metabolic activity of osteocytes, periostin, as the indicator of metabolic activity of periosteum and microRNAs as the group of specific markers in the early detection of osteoporosis. All of the above-mentioned candidates could possibly become a predictor of osteoporotic fractures: sclerostin in patients with type 2 diabetes; periostin, especially in non-vertebral fractures in postmenopausal women and microRNA in early prediction of these fractures. However, many of the studies underline some of the limitations associated with their use in the diagnosis of osteoporosis. Ambiguous results of the presented studies may be primarily due to population selection, population size, type of fractures and duration of the observation itself. An objective judgement will be made when an adequate number of standardized and independent studies will allow for the exclusion or validation of each of them in clinical practice.

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Sannicandro, Anthony J., Ana Soriano-Arroquia, and Katarzyna Goljanek-Whysall. "Micro(RNA)-managing muscle wasting." Journal of Applied Physiology 127, no. 2 (August 1, 2019): 619–32. http://dx.doi.org/10.1152/japplphysiol.00961.2018.

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Progressive skeletal muscle wasting is a natural consequence of aging and is common in chronic and acute diseases. Loss of skeletal muscle mass and function (strength) often leads to frailty, decreased independence, and increased risk of hospitalization. Despite progress made in our understanding of the mechanisms underlying muscle wasting, there is still no treatment available, with exercise training and dietary supplementation improving, but not restoring, muscle mass and/or function. There has been slow progress in developing novel therapies for muscle wasting, either during aging or disease, partially due to the complex nature of processes underlying muscle loss. The mechanisms of muscle wasting are multifactorial, with a combination of factors underlying age- and disease-related functional muscle decline. These factors include well-characterized changes in muscle such as changes in protein turnover and more recently described mechanisms such as autophagy or satellite cell senescence. Advances in transcriptomics and other high-throughput approaches have highlighted significant deregulation of skeletal muscle gene and protein levels during aging and disease. These changes are regulated at different levels, including posttranscriptional gene expression regulation by microRNAs. microRNAs, potent regulators of gene expression, modulate many processes in muscle, and microRNA-based interventions have been recently suggested as a promising new therapeutic strategy against alterations in muscle homeostasis. Here, we review recent developments in understanding the aging-associated mechanisms of muscle wasting and explore potential microRNA-based therapeutic avenues.

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Kataruka, Shubhangini, Martin Modrak, Veronika Kinterova, Radek Malik, Daniela M. Zeitler, Filip Horvat, Jiri Kanka, Gunter Meister, and Petr Svoboda. "MicroRNA dilution during oocyte growth disables the microRNA pathway in mammalian oocytes." Nucleic Acids Research 48, no. 14 (July 1, 2020): 8050–62. http://dx.doi.org/10.1093/nar/gkaa543.

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Abstract MicroRNAs (miRNAs) are ubiquitous small RNAs guiding post-transcriptional gene repression in countless biological processes. However, the miRNA pathway in mouse oocytes appears inactive and dispensable for development. We propose that marginalization of the miRNA pathway activity stems from the constraints and adaptations of RNA metabolism elicited by the diluting effects of oocyte growth. We report that miRNAs do not accumulate like mRNAs during the oocyte growth because miRNA turnover has not adapted to it. The most abundant miRNAs total tens of thousands of molecules in growing (∅ 40 μm) and fully grown (∅ 80 μm) oocytes, a number similar to that observed in much smaller fibroblasts. The lack of miRNA accumulation results in a 100-fold lower miRNA concentration in fully grown oocytes than in somatic cells. This brings a knock-down-like effect, where diluted miRNAs engage targets but are not abundant enough for significant repression. Low-miRNA concentrations were observed in rat, hamster, porcine and bovine oocytes, arguing that miRNA inactivity is not mouse-specific but a common mammalian oocyte feature. Injection of 250,000 miRNA molecules was sufficient to restore reporter repression in mouse and porcine oocytes, suggesting that miRNA inactivity comes from low-miRNA abundance and not from some suppressor of the pathway.

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Medina, Lisvaneth, Ana Liempi, Christian Castillo, Maura Rojas, Fernando Salomó, Alfredo Sepúlveda, and Ulrike Kemmerling. "Trypanosoma cruzi-induced trophoblast epithelial turnover is mediated by microRNA 515-5p." Placenta 112 (September 2021): e31. http://dx.doi.org/10.1016/j.placenta.2021.07.101.

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Gantier, Michael P., Claire E. McCoy, Mark A. Behlke, and Bryan R. G. Williams. "CS3-4 Characterisation of microRNA turnover reveals sustained modulation of innate immunity." Cytokine 52, no. 1-2 (October 2010): 38. http://dx.doi.org/10.1016/j.cyto.2010.07.159.

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Chen, Yu-Shan, Wei-Shiung Lian, Chung-Wen Kuo, Huei-Jing Ke, Shao-Yu Wang, Pei-Chen Kuo, Holger Jahr, and Feng-Sheng Wang. "Epigenetic Regulation of Skeletal Tissue Integrity and Osteoporosis Development." International Journal of Molecular Sciences 21, no. 14 (July 12, 2020): 4923. http://dx.doi.org/10.3390/ijms21144923.

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Bone turnover is sophisticatedly balanced by a dynamic coupling of bone formation and resorption at various rates. The orchestration of this continuous remodeling of the skeleton further affects other skeletal tissues through organ crosstalk. Chronic excessive bone resorption compromises bone mass and its porous microstructure as well as proper biomechanics. This accelerates the development of osteoporotic disorders, a leading cause of skeletal degeneration-associated disability and premature death. Bone-forming cells play important roles in maintaining bone deposit and osteoclastic resorption. A poor organelle machinery, such as mitochondrial dysfunction, endoplasmic reticulum stress, and defective autophagy, etc., dysregulates growth factor secretion, mineralization matrix production, or osteoclast-regulatory capacity in osteoblastic cells. A plethora of epigenetic pathways regulate bone formation, skeletal integrity, and the development of osteoporosis. MicroRNAs inhibit protein translation by binding the 3′-untranslated region of mRNAs or promote translation through post-transcriptional pathways. DNA methylation and post-translational modification of histones alter the chromatin structure, hindering histone enrichment in promoter regions. MicroRNA-processing enzymes and DNA as well as histone modification enzymes catalyze these modifying reactions. Gain and loss of these epigenetic modifiers in bone-forming cells affect their epigenetic landscapes, influencing bone homeostasis, microarchitectural integrity, and osteoporotic changes. This article conveys productive insights into biological roles of DNA methylation, microRNA, and histone modification and highlights their interactions during skeletal development and bone loss under physiological and pathological conditions.

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Podolska, Katerina, David Sedlak, Petr Bartunek, and Petr Svoboda. "Fluorescence-Based High-Throughput Screening of Dicer Cleavage Activity." Journal of Biomolecular Screening 19, no. 3 (August 14, 2013): 417–26. http://dx.doi.org/10.1177/1087057113497400.

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Production of small RNAs by ribonuclease III Dicer is a key step in microRNA and RNA interference pathways, which employ Dicer-produced small RNAs as sequence-specific silencing guides. Further studies and manipulations of microRNA and RNA interference pathways would benefit from identification of small-molecule modulators. Here, we report a study of a fluorescence-based in vitro Dicer cleavage assay, which was adapted for high-throughput screening. The kinetic assay can be performed under single-turnover conditions (35 nM substrate and 70 nM Dicer) in a small volume (5 µL), which makes it suitable for high-throughput screening in a 1536-well format. As a proof of principle, a small library of bioactive compounds was analyzed, demonstrating potential of the assay.

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Zhou, Jing, Yi-Shuan Li, Phu Nguyen, Kuei-Chun Wang, Anna Weiss, Yi-Chun Kuo, Jeng-Jiann Chiu, John Y. Shyy, and Shu Chien. "Regulation of Vascular Smooth Muscle Cell Turnover by Endothelial Cell–Secreted MicroRNA-126." Circulation Research 113, no. 1 (June 21, 2013): 40–51. http://dx.doi.org/10.1161/circresaha.113.280883.

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Perksanusak, T., K. Panyakhamlerd, N. Hirankarn, A. Suwan, A. Vasuratna, and N. Taechakraichana. "Correlation of plasma microRNA-21 expression and bone turnover markers in postmenopausal women." Climacteric 21, no. 6 (September 20, 2018): 581–85. http://dx.doi.org/10.1080/13697137.2018.1507020.

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Kocijan, Roland, Christian Muschitz, Elisabeth Geiger, Susanna Skalicky, Andreas Baierl, Rainer Dormann, Fabian Plachel, et al. "Circulating microRNA Signatures in Patients With Idiopathic and Postmenopausal Osteoporosis and Fragility Fractures." Journal of Clinical Endocrinology & Metabolism 101, no. 11 (August 23, 2016): 4125–34. http://dx.doi.org/10.1210/jc.2016-2365.

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Context: Established bone turnover markers do not reflect fracture risk in idiopathic male and premenopausal osteoporosis and the role of microRNAs (miRNAs) in these patients is currently unclear. miRNAs are a class of small non-coding RNAs that regulate gene expression and bone tissue homeostasis. They are considered a new class of endocrine regulators with promising potential as biomarkers. Objective: Evaluation of circulating miRNA signatures in male and female subjects with idiopathic and postmenopausal osteoporotic low-traumatic fractures. Design, Setting, and Patients: This was a case-control study of cross-sectional design of 36 patients with prevalent low-traumatic fractures and 39 control subjects Main Outcome Measures: One hundred eighty-seven miRNAs were quantified in serum by qPCR, compared between groups and correlated with established bone turnover markers. Results: Significant differences in serum levels of circulating miRNAs were identified in all three subgroups (46 in premenopausal, 52 in postmenopausal, 55 in male). A set of 19 miRNAs was consistently regulated in all three subgroups. Eight miRNAs [miR-152-3p, miR-30e-5p, miR-140-5p, miR-324-3p, miR-19b-3p, miR-335-5p, miR-19a-3p, miR-550a-3p] were excellent discriminators of patients with low-traumatic fractures, regardless of age and sex, with area under the curve values > 0.9. The 11 remaining miRNAs showed area under the curve values between 0.81 and 0.89. Correlation analysis identified significant correlations between miR-29b-3p and P1NP, and miR-365-5p and iPTH, TRAP5b, P1NP and Osteocalcin, as well as BMDL1–L4 and miR-19b-3p, miR-324-3p, miR-532-5p, and miR-93-5p. Conclusions: Specific serum miRNA profiles are strongly related to bone pathologies. Therefore miRNAs might be directly linked to bone tissue homeostasis. In particular, miR-29b-3p has previously been reported as regulator of osteogenic differentiation and could serve as a novel marker of bone turnover in osteoporotic patients as a member of a miRNA signature.

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Kim, Jeong-Min, Kwang-Yeol Park, Hye Ryoun Kim, Hwa Young Ahn, Leonardo Pantoni, Moo-Seok Park, Su-Hyun Han, Hae-Bong Jung, and Jaehan Bae. "Association of Bone Mineral Density to Cerebral Small Vessel Disease Burden." Neurology 96, no. 9 (January 11, 2021): e1290-e1300. http://dx.doi.org/10.1212/wnl.0000000000011526.

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ObjectiveTo test the hypothesis that bone mineral loss is mechanistically related to cerebral small vessel disease (SVD), we investigated the relationship between bone mineral density and the prevalence and intensity of SVD among patients with stroke.MethodsWe analyzed data of 1,190 consecutive patients with stroke who were >50 years of age and underwent both brain MRI and dual-energy x-ray absorptiometry from the stroke registry of Chung-Ang University Hospital in Seoul, Korea. The patients were categorized into 3 groups according to their bone mineral density (normal, osteopenia, and osteoporosis). White matter hyperintensities, silent lacunes, cerebral microbleeds, and extensive perivascular space were assessed from brain MRI. Multinomial logistic regression model was used to examine the association between osteoporosis and total SVD score. We also recruited 70 patients with stroke to study serum bone turnover markers and microRNAs related to both cerebral atherosclerosis and bone metabolism to understand bone and brain interaction.ResultsOsteoporosis was determined among 284 patients (23.9%), and 450 patients (37.8%) had osteopenia. As bone mineral density decreased, total SVD score and the incidence of every SVD phenotype increased except strictly lobar cerebral microbleeds. Multinomial logistic regression analysis showed that osteoporosis was independently associated with severe SVD burden. The levels of microRNA-378f were significantly increased among the patients with osteoporosis and maximal total SVD score and positively correlated with parathyroid hormone and osteocalcin.ConclusionsThese findings suggest a pathophysiologic link between bone mineral loss and hypertensive cerebral arteriolar degeneration, possibly mediated by circulating microRNA.

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Razny, Urszula, Anna Polus, Joanna Goralska, Anna Zdzienicka, Anna Gruca, Maria Kapusta, Maria Biela, Aldona Dembinska-Kiec, Bogdan Solnica, and Malgorzata Malczewska-Malec. "Effect of insulin resistance on whole blood mRNA and microRNA expression affecting bone turnover." European Journal of Endocrinology 181, no. 5 (November 2019): 525–37. http://dx.doi.org/10.1530/eje-19-0542.

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Objective To evaluate the effect of insulin resistance in obesity on the expression in whole blood of mRNA and miRNA affecting bone homeostasis as well as to estimate the influence of oral glucose load (OGTT) on serum osteocalcin concentration in obese individuals with and without insulin resistance. Design Cross-sectional study. Methods Carboxylated (cOC), undercarboxylated (ucOC) and total osteocalcin were measured by ELISA in the serum of obese subjects with insulin resistance (n = 41) and obese subjects without insulin resistance (n = 41) (control group) during OGTT. Analysis of gene expression (microarray) and miRNAs (real-time PCR) was performed in venous blood (representating samples) collected before OGTT from obese with insulin resistance and controls. Results Obese subjects with insulin resistance (higher HOMA-IR and lower oral glucose insulin sensitivity index) presented significantly increased expression of WNT signalling inhibitors (DKK1, DKK2, SOST, SFRP1) and downregulation of the key factor in WNT signalling – β catenin participating in osteoblasts differentiation. Expression of miRNA involved in osteoblastogenesis was also inhibited (miR-29b, miR-181a, miR-210, miR-324-3p). During OGTT, contrary to the control group, subjects with insulin resistance presented suppression of cOC and total OC decrease after 1 and 2 h of oral glucose load. Conclusions Obese subjects with insulin resistance may have defects in osteoblastogenesis that was demonstrated via key signalling molecules mRNA downregulation, and increased expression of WNT antagonists as well as inhibition of expression of miRNA participating in the regulation of osteoblast differentiation. Disturbed osteoblastogenesis in insulin-resistant subjects results in the suppression of blood carboxylated and total osteocalcin decrease during OGTT.

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Xian, Liman, Feng Xu, Jianzhou Liu, Ning Xu, Haidong Li, Haoying Ge, Kun Shao, Jiangli Fan, Guishan Xiao, and Xiaojun Peng. "MicroRNA Detection with Turnover Amplification via Hybridization-Mediated Staudinger Reduction for Pancreatic Cancer Diagnosis." Journal of the American Chemical Society 141, no. 51 (November 27, 2019): 20490–97. http://dx.doi.org/10.1021/jacs.9b11272.

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Wu, Haoxing, Brandon T. Cisneros, Christian M. Cole, and Neal K. Devaraj. "Bioorthogonal Tetrazine-Mediated Transfer Reactions Facilitate Reaction Turnover in Nucleic Acid-Templated Detection of MicroRNA." Journal of the American Chemical Society 136, no. 52 (December 19, 2014): 17942–45. http://dx.doi.org/10.1021/ja510839r.

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Tu, Bin, Li Liu, Chi Xu, Jixian Zhai, Shengben Li, Miguel A. Lopez, Yuanyuan Zhao, et al. "Distinct and Cooperative Activities of HESO1 and URT1 Nucleotidyl Transferases in MicroRNA Turnover in Arabidopsis." PLOS Genetics 11, no. 4 (April 30, 2015): e1005119. http://dx.doi.org/10.1371/journal.pgen.1005119.

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Kretov, Dmitry A., Isha A. Walawalkar, Alexandra Mora-Martin, Andrew M. Shafik, Simon Moxon, and Daniel Cifuentes. "Ago2-Dependent Processing Allows miR-451 to Evade the Global MicroRNA Turnover Elicited during Erythropoiesis." Molecular Cell 78, no. 2 (April 2020): 317–28. http://dx.doi.org/10.1016/j.molcel.2020.02.020.

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Chakrabarty, Yogaditya, and Suvendra N. Bhattacharyya. "Leishmania donovani restricts mitochondrial dynamics to enhance miRNP stability and target RNA repression in host macrophages." Molecular Biology of the Cell 28, no. 15 (July 15, 2017): 2091–105. http://dx.doi.org/10.1091/mbc.e16-06-0388.

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MicroRNAs (miRNAs), the tiny regulatory RNAs, form complexes with Argonaute (Ago) proteins and inhibit gene expression in metazoan cells. While studying parasite-invaded macrophages, we identify a unique mode of gene regulation in which the parasite Leishmania donovani (Ld) causes mitochondrial depolarization, reduces mitochondrial dynamics, and restricts turnover of cellular microRNA ribonucleoprotein (miRNP) complexes in infected host cells. This leads to increased stability of miRNPs along with elevated levels of Ago2-bound cytokine mRNA in Ld-infected macrophages. Thus the increase of miRNP stability in Ld-infected cells curtails production of proinflammatory cytokines, which are otherwise detrimental for survival of the parasite within the infected macrophages. Loss of mitochondrial membrane potential is accompanied by reduced juxtaposition of endoplasmic reticulum (ER) and mitochondria as well as endosomes. This is likely coupled with enhanced sequestration and stabilization of ER- associated miRNPs observed in infected macrophage cells. Mitofusin 2 (Mfn2), a membrane protein implicated in ER–mitochondria tethering, also shows reduced expression in Ld-infected cells. A mitochondrial role in Ld-induced alteration of miRNA activity and stability is further corroborated by impaired compartmentalization and stabilization of miRNP components in Mfn2-depleted mammalian cells.

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Zhu, Juan-Juan, Yue-Feng Liu, Yun-Peng Zhang, Chuan-Rong Zhao, Wei-Juan Yao, Yi-Shuan Li, Kuei-Chun Wang, et al. "VAMP3 and SNAP23 mediate the disturbed flow-induced endothelial microRNA secretion and smooth muscle hyperplasia." Proceedings of the National Academy of Sciences 114, no. 31 (July 17, 2017): 8271–76. http://dx.doi.org/10.1073/pnas.1700561114.

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Vascular endothelial cells (ECs) at arterial branches and curvatures experience disturbed blood flow and induce a quiescent-to-activated phenotypic transition of the adjacent smooth muscle cells (SMCs) and a subsequent smooth muscle hyperplasia. However, the mechanism underlying the flow pattern-specific initiation of EC-to-SMC signaling remains elusive. Our previous study demonstrated that endothelial microRNA-126-3p (miR-126-3p) acts as a key intercellular molecule to increase turnover of the recipient SMCs, and that its release is reduced by atheroprotective laminar shear (12 dynes/cm2) to ECs. Here we provide evidence that atherogenic oscillatory shear (0.5 ± 4 dynes/cm2), but not atheroprotective pulsatile shear (12 ± 4 dynes/cm2), increases the endothelial secretion of nonmembrane-bound miR-126-3p and other microRNAs (miRNAs) via the activation of SNAREs, vesicle-associated membrane protein 3 (VAMP3) and synaptosomal-associated protein 23 (SNAP23). Knockdown of VAMP3 and SNAP23 reduces endothelial secretion of miR-126-3p and miR-200a-3p, as well as the proliferation, migration, and suppression of contractile markers in SMCs caused by EC-coculture. Pharmacological intervention of mammalian target of rapamycin complex 1 in ECs blocks endothelial secretion and EC-to-SMC transfer of miR-126-3p through transcriptional inhibition of VAMP3 and SNAP23. Systemic inhibition of VAMP3 and SNAP23 by rapamycin or periadventitial application of the endocytosis inhibitor dynasore ameliorates the disturbed flow-induced neointimal formation, whereas intraluminal overexpression of SNAP23 aggravates it. Our findings demonstrate the flow-pattern–specificity of SNARE activation and its contribution to the miRNA-mediated EC–SMC communication.

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Pedersen, Oliver Buchhave, Anne-Mette Hvas, Erik Lerkevang Grove, Sanne Bøjet Larsen, Leonardo Pasalic, Steen Dalby Kristensen, and Peter H. Nissen. "Association of whole blood microRNA expression with platelet function and turnover in patients with coronary artery disease." Thrombosis Research 211 (March 2022): 98–105. http://dx.doi.org/10.1016/j.thromres.2022.01.026.

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Zhai, Yuxin, Zhenping Zhong, Chyi-Ying A. Chen, Zhenfang Xia, Ling Song, Michael R. Blackburn, and Ann-Bin Shyu. "Coordinated Changes in mRNA Turnover, Translation, and RNA Processing Bodies in Bronchial Epithelial Cells following Inflammatory Stimulation." Molecular and Cellular Biology 28, no. 24 (October 20, 2008): 7414–26. http://dx.doi.org/10.1128/mcb.01237-08.

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ABSTRACT Bronchial epithelial cells play a pivotal role in airway inflammation, but little is known about posttranscriptional regulation of mediator gene expression during the inflammatory response in these cells. Here, we show that activation of human bronchial epithelial BEAS-2B cells by proinflammatory cytokines interleukin-4 (IL-4) and tumor necrosis factor alpha (TNF-α) leads to an increase in the mRNA stability of the key chemokines monocyte chemotactic protein 1 and IL-8, an elevation of the global translation rate, an increase in the levels of several proteins critical for translation, and a reduction of microRNA-mediated translational repression. Moreover, using the BEAS-2B cell system and a mouse model, we found that RNA processing bodies (P bodies), cytoplasmic domains linked to storage and/or degradation of translationally silenced mRNAs, are significantly reduced in activated bronchial epithelial cells, suggesting a physiological role for P bodies in airway inflammation. Our study reveals an orchestrated change among posttranscriptional mechanisms, which help sustain high levels of inflammatory mediator production in bronchial epithelium during the pathogenesis of inflammatory airway diseases.

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Akira, Shizuo, and Kazuhiko Maeda. "Control of RNA Stability in Immunity." Annual Review of Immunology 39, no. 1 (April 26, 2021): 481–509. http://dx.doi.org/10.1146/annurev-immunol-101819-075147.

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Posttranscriptional control of mRNA regulates various biological processes, including inflammatory and immune responses. RNA-binding proteins (RBPs) bind cis-regulatory elements in the 3′ untranslated regions (UTRs) of mRNA and regulate mRNA turnover and translation. In particular, eight RBPs (TTP, AUF1, KSRP, TIA-1/TIAR, Roquin, Regnase, HuR, and Arid5a) have been extensively studied and are key posttranscriptional regulators of inflammation and immune responses. These RBPs sometimes collaboratively or competitively bind the same target mRNA to enhance or dampen regulatory activities. These RBPs can also bind their own 3′ UTRs to negatively or positively regulate their expression. Both upstream signaling pathways and microRNA regulation shape the interactions between RBPs and target RNA. Dysregulation of RBPs results in chronic inflammation and autoimmunity. Here, we summarize the functional roles of these eight RBPs in immunity and their associated diseases.

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de Morree, Antoine, Julian D. D. Klein, Qiang Gan, Jean Farup, Andoni Urtasun, Abhijnya Kanugovi, Biter Bilen, Cindy T. J. van Velthoven, Marco Quarta, and Thomas A. Rando. "Alternative polyadenylation of Pax3 controls muscle stem cell fate and muscle function." Science 366, no. 6466 (November 7, 2019): 734–38. http://dx.doi.org/10.1126/science.aax1694.

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Adult stem cells are essential for tissue homeostasis. In skeletal muscle, muscle stem cells (MuSCs) reside in a quiescent state, but little is known about the mechanisms that control homeostatic turnover. Here we show that, in mice, the variation in MuSC activation rate among different muscles (for example, limb versus diaphragm muscles) is determined by the levels of the transcription factor Pax3. We further show that Pax3 levels are controlled by alternative polyadenylation of its transcript, which is regulated by the small nucleolar RNA U1. Isoforms of the Pax3 messenger RNA that differ in their 3′ untranslated regions are differentially susceptible to regulation by microRNA miR206, which results in varying levels of the Pax3 protein in vivo. These findings highlight a previously unrecognized mechanism of the homeostatic regulation of stem cell fate by multiple RNA species.

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Reddy, Sushma, Mingming Zhao, Dong-Qing Hu, Giovanni Fajardo, Shijun Hu, Zhumur Ghosh, Viswanathan Rajagopalan, Joseph C. Wu, and Daniel Bernstein. "Dynamic microRNA expression during the transition from right ventricular hypertrophy to failure." Physiological Genomics 44, no. 10 (May 15, 2012): 562–75. http://dx.doi.org/10.1152/physiolgenomics.00163.2011.

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MicroRNAs (miRs) are small, noncoding RNAs that are emerging as crucial regulators of cardiac remodeling in left ventricular hypertrophy (LVH) and failure (LVF). However, there are no data on their role in right ventricular hypertrophy (RVH) and failure (RVF). This is a critical question given that the RV is uniquely at risk in patients with congenital right-sided obstructive lesions and in those with systemic RVs. We have developed a murine model of RVH and RVF using pulmonary artery constriction (PAC). miR microarray analysis of RV from PAC vs. control demonstrates altered miR expression with gene targets associated with cardiomyocyte survival and growth during hypertrophy (miR 199a-3p) and reactivation of the fetal gene program during heart failure (miR-208b). The transition from hypertrophy to heart failure is characterized by apoptosis and fibrosis (miRs-34, 21, 1). Most are similar to LVH/LVF. However, there are several key differences between RV and LV: four miRs (34a, 28, 148a, and 93) were upregulated in RVH/RVF that are downregulated or unchanged in LVH/LVF. Furthermore, there is a corresponding downregulation of their putative target genes involving cell survival, proliferation, metabolism, extracellular matrix turnover, and impaired proteosomal function. The current study demonstrates, for the first time, alterations in miRs during the process of RV remodeling and the gene regulatory pathways leading to RVH and RVF. Many of these alterations are similar to those in the afterload-stressed LV. miRs differentially regulated between the RV and LV may contribute to the RVs increased susceptibility to heart failure.

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Park, Jong Kook, Han Peng, Julia Katsnelson, Wending Yang, Nihal Kaplan, Ying Dong, Joshua Z. Rappoport, CongCong He, and Robert M. Lavker. "MicroRNAs-103/107 coordinately regulate macropinocytosis and autophagy." Journal of Cell Biology 215, no. 5 (November 21, 2016): 667–85. http://dx.doi.org/10.1083/jcb.201604032.

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Macropinocytosis, by which cells ingest large amounts of fluid, and autophagy, the lysosome-based catabolic process, involve vesicular biogenesis (early stage) and turnover (end stage). Much is known about early-stage events; however, our understanding of how the end stages of these processes are governed is incomplete. Here we demonstrate that the microRNA-103/107(miR-103/107) family, which is preferentially expressed in the stem cell–enriched limbal epithelium, coordinately regulates aspects of both these activities. Loss of miR-103/107 causes dysregulation of macropinocytosis with the formation of large vacuoles, primarily through up-regulation of Src, Ras, and Ankfy1. Vacuole accumulation is not a malfunction of early-stage autophagy; rather, miR-103/107 ensure proper end-stage autophagy by regulating diacylglycerol/protein kinase C and cyclin-dependent kinase 5 signaling, which enables dynamin to function in vacuole clearance. Our findings unveil a key biological function for miR-103/107 in coordinately suppressing macropinocytosis and preserving end-stage autophagy, thereby contributing to maintenance of a stem cell–enriched epithelium.

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Bronevetsky, Yelena, Alejandro V. Villarino, Christopher J. Eisley, Rebecca Barbeau, Andrea J. Barczak, Gitta A. Heinz, Elisabeth Kremmer, et al. "T cell activation induces proteasomal degradation of Argonaute and rapid remodeling of the microRNA repertoire." Journal of Experimental Medicine 210, no. 2 (February 4, 2013): 417–32. http://dx.doi.org/10.1084/jem.20111717.

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Activation induces extensive changes in the gene expression program of naive CD4+ T cells, promoting their differentiation into helper T cells that coordinate immune responses. MicroRNAs (miRNAs) play a critical role in this process, and miRNA expression also changes dramatically during T cell differentiation. Quantitative analyses revealed that T cell activation induces global posttranscriptional miRNA down-regulation in vitro and in vivo. Argonaute (Ago) proteins, the core effector proteins of the miRNA-induced silencing complex (miRISC), were also posttranscriptionally down-regulated during T cell activation. Ago2 was inducibly ubiquitinated in activated T cells and its down-regulation was inhibited by the proteasome inhibitor MG132. Therefore, activation-induced miRNA down-regulation likely occurs at the level of miRISC turnover. Measurements of miRNA-processing intermediates uncovered an additional layer of activation-induced, miRNA-specific transcriptional regulation. Thus, transcriptional and posttranscriptional mechanisms cooperate to rapidly reprogram the miRNA repertoire in differentiating T cells. Altering Ago2 expression in T cells revealed that Ago proteins are limiting factors that determine miRNA abundance. Naive T cells with reduced Ago2 and miRNA expression differentiated more readily into cytokine-producing helper T cells, suggesting that activation-induced miRNA down-regulation promotes acquisition of helper T cell effector functions by relaxing the repression of genes that direct T cell differentiation.

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Miki, Takashi S., Stefan Rüegger, Dimos Gaidatzis, Michael B. Stadler, and Helge Großhans. "Engineering of a conditional allele reveals multiple roles of XRN2 in Caenorhabditis elegans development and substrate specificity in microRNA turnover." Nucleic Acids Research 42, no. 6 (January 20, 2014): 4056–67. http://dx.doi.org/10.1093/nar/gkt1418.

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Mukherjee, Sromana, Nuria Paricio, and Nicholas S. Sokol. "A stress-responsive miRNA regulates BMP signaling to maintain tissue homeostasis." Proceedings of the National Academy of Sciences 118, no. 21 (May 20, 2021): e2022583118. http://dx.doi.org/10.1073/pnas.2022583118.

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Adult organisms must sense and adapt to environmental fluctuations. In high-turnover tissues such as the intestine, these adaptive responses require rapid changes in gene expression that, in turn, likely involve posttranscriptional gene control. However, intestinal-tissue–specific microRNA (miRNA)-mediated regulatory pathways remain unexplored. Here, we report the role of an intestinal-specific miRNA, miR-958, that non–cell autonomously regulates stem cell numbers during tissue homeostasis and regeneration in the Drosophila adult midgut. We identify its downstream target cabut, the Drosophila ortholog of mammalian KLF10/11 transcription factors, which mediates this miR-958 function by promoting paracrine enterocyte-to-stem-cell bone morphogenetic protein (BMP) signaling. We also show that mature miR-958 levels transiently decrease in response to stress and that this decrease is required for proper stem cell expansion during tissue regeneration. In summary, we have identified a posttranscriptional mechanism that modulates BMP signaling activity within Drosophila adult intestinal tissue during both normal homeostasis and tissue regeneration to regulate intestinal stem cell numbers.

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Burger, Kaspar, Margarita Schlackow, Martin Potts, Svenja Hester, Shabaz Mohammed, and Monika Gullerova. "Nuclear phosphorylated Dicer processes double-stranded RNA in response to DNA damage." Journal of Cell Biology 216, no. 8 (June 22, 2017): 2373–89. http://dx.doi.org/10.1083/jcb.201612131.

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The endoribonuclease Dicer is a key component of the human RNA interference pathway and is known for its role in cytoplasmic microRNA production. Recent findings suggest that noncanonical Dicer generates small noncoding RNA to mediate the DNA damage response (DDR). Here, we show that human Dicer is phosphorylated in the platform–Piwi/Argonaute/Zwille–connector helix cassette (S1016) upon induction of DNA damage. Phosphorylated Dicer (p-Dicer) accumulates in the nucleus and is recruited to DNA double-strand breaks. We further demonstrate that turnover of damage-induced nuclear, double-stranded (ds) RNA requires additional phosphorylation of carboxy-terminal Dicer residues (S1728 and S1852). DNA damage-induced nuclear Dicer accumulation is conserved in mammals. Dicer depletion causes endogenous DNA damage and delays the DDR by impaired recruitment of repair factors MDC1 and 53BP1. Collectively, we place Dicer within the context of the DDR by demonstrating a DNA damage-inducible phosphoswitch that causes localized processing of nuclear dsRNA by p-Dicer to promote DNA repair.

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Zhu, Yunxia, Yi Sun, Yuncai Zhou, Yan Zhang, Tao Zhang, Yating Li, Weiyan You, Xiaoai Chang, Li Yuan, and Xiao Han. "MicroRNA-24 promotes pancreatic beta cells toward dedifferentiation to avoid endoplasmic reticulum stress-induced apoptosis." Journal of Molecular Cell Biology 11, no. 9 (February 12, 2019): 747–60. http://dx.doi.org/10.1093/jmcb/mjz004.

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AbstractCurrent research indicates that beta cell loss in type 2 diabetes may be attributed to beta cell dedifferentiation rather than apoptosis; however, the mechanisms by which this occurs remain poorly understood. Our previous study demonstrated that elevation of microRNA-24 (miR-24) in a diabetic setting caused beta cell dysfunction and replicative deficiency. In this study, we focused on the role of miR-24 in beta cell apoptosis and dedifferentiation under endoplasmic reticulum (ER) stress conditions. We found that miR-24 overabundance protected beta cells from thapsigargin-induced apoptosis at the cost of accelerating the impairment of glucose-stimulated insulin secretion (GSIS) and enhancing the presence of dedifferentiation markers. Ingenuity® Pathway Analysis (IPA) revealed that elevation of miR-24 had an inhibitory effect on XBP1 and ATF4, which are downstream effectors of two key branches of ER stress, by inhibiting its direct target, Ire1α. Notably, elevated miR-24 initiated another pathway that targeted Mafa and decreased GSIS function in surviving beta cells, thus guiding their dedifferentiation under ER stress conditions. Our results demonstrated that the elevated miR-24, to the utmost extent, preserves beta cell mass by inhibiting apoptosis and inducing dedifferentiation. This study not only provides a novel mechanism by which miR-24 dominates beta cell turnover under persistent metabolic stress but also offers a therapeutic consideration for treating diabetes by inducing dedifferentiated beta cells to re-differentiation.

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Norbury, Chris J. "3′ uridylation and the regulation of RNA function in the cytoplasm." Biochemical Society Transactions 38, no. 4 (July 26, 2010): 1150–53. http://dx.doi.org/10.1042/bst0381150.

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Degradation of cytoplasmic mRNAs is an important aspect of the regulation of gene function in eukaryotes. Much of what is currently known about the underlying pathways of mRNA decay is derived from studies of the budding yeast Saccharomyces cerevisiae, in which mRNA turnover is initiated by deadenylation, followed either by decapping and 5′→3′ degradation or by further 3′→5′ exonucleolysis. Our studies using RNA cRACE (circularization-based rapid amplification of cDNA ends) techniques indicate that mRNA decapping in the fission yeast Schizosaccharomyces pombe often does not require prior deadenylation. Furthermore, the poly(A) polymerase-related, cytoplasmic enzyme Cid1 catalyses uridylation of a variety of functionally diverse poly(A)+ mRNAs and hence stimulates decapping as part of a novel mRNA turnover pathway. The pathways initiated by uridylation and deadenylation stimulate decapping in a partially redundant fashion, but urg1 mRNA is stabilized in mutants lacking cid1. Accumulation of uridylated RNAs in an lsm1 mutant suggests an involvement of the Lsm1–7 complex in recognition of the 3′ uridylation tag and recruitment of the decapping machinery. Recent reports from other groups suggest that in metazoans, which unlike budding yeast contain Cid1 orthologues, 3′ uridylation by such enzymes is used to regulate miRNA (microRNA) and siRNA (small interfering RNA) biogenesis and activity. It has further been suggested that uridylation is an important regulatory modification of non-polyadenylated replication-dependent histone mRNAs. This modification may also form the basis of a widespread mechanism for the initiation of the decay of polyadenylated mRNAs in organisms other than fission yeast.

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Degani, Neta, Yoav Lubelsky, Rotem Ben-Tov Perry, Elena Ainbinder, and Igor Ulitsky. "Highly conserved and cis-acting lncRNAs produced from paralogous regions in the center of HOXA and HOXB clusters in the endoderm lineage." PLOS Genetics 17, no. 7 (July 19, 2021): e1009681. http://dx.doi.org/10.1371/journal.pgen.1009681.

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Long noncoding RNAs (lncRNAs) have been shown to play important roles in gene regulatory networks acting in early development. There has been rapid turnover of lncRNA loci during vertebrate evolution, with few human lncRNAs conserved beyond mammals. The sequences of these rare deeply conserved lncRNAs are typically not similar to each other. Here, we characterize HOXA-AS3 and HOXB-AS3, lncRNAs produced from the central regions of the HOXA and HOXB clusters. Sequence-similar orthologs of both lncRNAs are found in multiple vertebrate species and there is evident sequence similarity between their promoters, suggesting that the production of these lncRNAs predates the duplication of the HOX clusters at the root of the vertebrate lineage. This conservation extends to similar expression patterns of the two lncRNAs, in particular in cells transiently arising during early development or in the adult colon. Functionally, the RNA products of HOXA-AS3 and HOXB-AS3 regulate the expression of their overlapping HOX5–7 genes both in HT-29 cells and during differentiation of human embryonic stem cells. Beyond production of paralogous protein-coding and microRNA genes, the regulatory program in the HOX clusters therefore also relies on paralogous lncRNAs acting in restricted spatial and temporal windows of embryonic development and cell differentiation.

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Zou, Lingyue, Wenqiang Bao, Yadong Gao, Mengting Chen, Yajiao Wu, Shuo Wang, Chutao Li, et al. "Integrated Analysis of Transcriptome and microRNA Profile Reveals the Toxicity of Euphorbia Factors toward Human Colon Adenocarcinoma Cell Line Caco-2." Molecules 27, no. 20 (October 16, 2022): 6931. http://dx.doi.org/10.3390/molecules27206931.

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Euphorbia factors, lathyrane-type diterpenoids isolated from the medical herb Euphorbia lathyris L. (Euphorbiaceae), have been associated with intestinal irritation toxicity, but the mechanisms underlying this phenomenon are still unknown. The objective of this study was to evaluate the transcriptome and miRNA profiles of human colon adenocarcinoma Caco-2 cells in response to Euphorbia factors L1 (EFL1) and EFL2. Whole transcriptomes of mRNA and microRNA (miRNA) were obtained using second generation high-throughput sequencing technology in response to 200 μM EFL treatment for 72 h, and the differentially expressed genes and metabolism pathway were enriched. Gene structure changes were analyzed by comparing them with reference genome sequences. After 72 h of treatment, 16 miRNAs and 154 mRNAs were differently expressed between the EFL1 group and the control group, and 47 miRNAs and 1101 mRNAs were differentially expressed between the EFL2 group and the control. Using clusters of orthologous protein enrichment, the sequenced mRNAs were shown to be mainly involved in transcription, post-translational modification, protein turnover, chaperones, signal transduction mechanisms, intracellular trafficking, secretion, vesicular transport, and the cytoskeleton. The differentially expressed mRNA functions and pathways were enriched in transmembrane transport, T cell extravasation, the IL-17 signaling pathway, apoptosis, and the cell cycle. The differentially expressed miRNA EFLs caused changes in the structure of the gene, including alternative splicing, insertion and deletion, and single nucleotide polymorphisms. This study reveals the underlying mechanism responsible for the toxicity of EFLs in intestinal cells based on transcriptome and miRNA profiles of gene expression and structure.

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Danilevicz, Monica, Kanhu Moharana, Thiago Venancio, Luciana Franco, Sérgio Cardoso, Mônica Cardoso, Flávia Thiebaut, Adriana Hemerly, Francisco Prosdocimi, and Paulo Ferreira. "Copaifera langsdorffii Novel Putative Long Non-Coding RNAs: Interspecies Conservation Analysis in Adaptive Response to Different Biomes." Non-Coding RNA 4, no. 4 (October 8, 2018): 27. http://dx.doi.org/10.3390/ncrna4040027.

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Long non-coding RNAs (lncRNAs) are involved in multiple regulatory pathways and its versatile form of action has disclosed a new layer in gene regulation. LncRNAs have their expression levels modulated during plant development, and in response to stresses with tissue-specific functions. In this study, we analyzed lncRNA from leaf samples collected from the legume Copaifera langsdorffii Desf. (copaíba) present in two divergent ecosystems: Cerrado (CER; Ecological Station of Botanical Garden in Brasília, Brazil) and Atlantic Rain Forest (ARF; Rio de Janeiro, Brazil). We identified 8020 novel lncRNAs, and they were compared to seven Fabaceae genomes and transcriptomes, to which 1747 and 2194 copaíba lncRNAs were mapped, respectively, to at least one species. The secondary structures of the lncRNAs that were conserved and differentially expressed between the populations were predicted using in silico methods. A few selected lncRNA were confirmed by RT-qPCR in the samples from both biomes; Additionally, the analysis of the lncRNA sequences predicted that some might act as microRNA (miRNA) targets or decoys. The emerging studies involving lncRNAs function and conservation have shown their involvement in several types of biotic and abiotic stresses. Thus, the conservation of lncRNAs among Fabaceae species considering their rapid turnover, suggests they are likely to have been under functional conservation pressure. Our results indicate the potential involvement of lncRNAs in the adaptation of C. langsdorffii in two different biomes.

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Gangula, Pandu R., Kishore B. Challagundla, Kalpana Ravella, Sutapa Mukhopadhyay, Vijayakumar Chinnathambi, Mukul K. Mittal, K. Raja Sekhar, and Chethan Sampath. "Sepiapterin alleviates impaired gastric nNOS function in spontaneous diabetic female rodents through NRF2 mRNA turnover and miRNA biogenesis pathway." American Journal of Physiology-Gastrointestinal and Liver Physiology 315, no. 6 (December 1, 2018): G980—G990. http://dx.doi.org/10.1152/ajpgi.00152.2018.

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An impaired nitrergic system and altered redox signaling contribute to gastric dysmotility in diabetics. Our earlier studies show that NF-E2-related factor 2 (NRF2) and phase II antioxidant enzymes play a vital role in gastric neuronal nitric oxide synthase (nNOS) function. This study aims to investigate whether supplementation of sepiapterin (SEP), a precursor for tetrahydrobiopterin (BH4) (a cofactor of NOS) via the salvage pathway, restores altered nitrergic systems and redox balance in spontaneous diabetic (DB) female rats. Twelve-week spontaneous DB and age-matched, non-DB rats, with and without dietary SEP (daily 20 mg/kg body wt for 10 days) treatment, were used in this study. Gastric antrum muscular tissues were excised to investigate the effects of SEP in nitrergic relaxation and the nNOS-nitric oxide (NO)-NRF2 pathway(s). Dietary SEP supplementation significantly ( P < 0.05) reverted diabetes-induced changes in nNOS dimerization and function; nitric oxide (NO) downstream signaling molecules; HSP-90, a key regulator of nNOSα activity and dimerization; miRNA-28 that targets NRF2 messenger RNA (mRNA), and levels of microRNA (miRNA) biogenesis pathway components, such as DGCR8 (DiGeorge Syndrome Critical Region Gene 8) and TRBP (HIV1-1 transactivating response RNA-binding protein). These findings emphasize the importance of the BH4 pathway in regulating gastric motility functions in DB animals by modulating nNOSα dimerization in association with changes in enteric NRF2 and NO downstream signaling. Our results also identify a new pathway, wherein SEP regulates NRF2 mRNA turnover by suppressing elevated miRNA-28, which could be related to alterations in miRNA biogenesis pathway components. NEW & NOTEWORTHY This study is the first to show a causal link between NF-E2-related factor 2 (NRF2) and neuronal nitric oxide synthase (nNOS) in gastric motility function. Our data demonstrate that critical regulators of the miRNA biosynthetic pathway are upregulated in the diabetic (DB) setting; these regulators were rescued by sepiapterin (SEP) treatment. Finally, we show that low dihydrofolate reductase expression may lead to impaired nNOS dimerization/function-reduced nitric oxide downstream signaling and elevate oxidative stress by suppressing the NRF2/phase II pathway through miRNA; SEP treatment restored all of the above in DB gastric muscular tissue. We suggest that tetrahydrobiopterin supplementation may be a useful therapy for patients with diabetes, as well as women with idiopathic gastroparesis.

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Journal articles on the topic 'MicroRNA turnover'

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