Journal articles: 'MiR-9a'

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Wang, Ning, Lei Yang, Huixue Zhang, Xiaoyu Lu, Jianjian Wang, Yuze Cao, Lixia Chen, et al. "MicroRNA-9a-5p Alleviates Ischemia Injury After Focal Cerebral Ischemia of the Rat by Targeting ATG5-Mediated Autophagy." Cellular Physiology and Biochemistry 45, no. 1 (December 22, 2017): 78–87. http://dx.doi.org/10.1159/000486224.

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Background/Aims: Previous studies have suggested that autophagy is activated in distinct cerebrovascular diseases, including stroke. However, the underlying regulatory mechanism of autophagy under stroke remained elusive. Accumulating evidence indicates that dysfunctions of microRNAs (miRNAs) are involved in the pathological process of stroke. Therefore, this study was taken to identify the effect of microRNA-9a-5p (miR-9a-5p) on autophagy in rats following stroke. Methods: The rat model of focal cerebral ischemia was established by middle cerebral artery occlusion (MCAO) surgery; The neurological outcomes were defined by neurological evaluation and infarct volume; The western blotting and immunofluorescence assays were used to detected the protein levels of microtubule-associated protein 1 light chain 3 (LC3) and autophagy related 5 (ATG5); The mRNA level of miR-9a-5p, LC3 and ATG5 were quantified by real-time RT-PCR; The luciferase activities of ATG5 and miR-9a-5p was detected by luciferase assay. Results: We showed here that the level of miR-9a-5p was decreased in the ischemic region of rats after MCAO. Overexpression of miR-9a-5p by miR-9a-5p agomir reduced infarct volume and alleviated neurological deficit. Moreover, we found that autophagy was activated by miR-9a-5p inhibition and inactivated by miR-9a-5p overexpression both in the MCAO rat and in SY-5Y cell lines, and unchanged by miR-masks as indicated by LC3 expression. Furthermore, the protein level of ATG5 was decreased by miR-9a-5p overexpression, but increased by miR-9a-5p inhibition and unchanged by miR-masks transfection. In addition, the luciferase assay data showed that miR-9a-5p suppressed the luciferase activity of 3’UTR of ATG5, whereas the repressive effect was relieved by mutation of binding sites. Conclusion: Our study demonstrated that miR-9a-5p may play a critical role in regulating the process of autophagy through targeting ATG5 expression, and overexpression of miR-9a-5p may be a potential approach in alleviating ischemia injury induced by MCAO.

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Gallicchio, Lorenzo, Sam Griffiths-Jones, and Matthew Ronshaugen. "Single-cell visualization of mir-9a and Senseless co-expression during Drosophila melanogaster embryonic and larval peripheral nervous system development." G3 Genes|Genomes|Genetics 11, no. 1 (December 22, 2020): 1–11. http://dx.doi.org/10.1093/g3journal/jkaa010.

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Abstract The Drosophila melanogaster peripheral nervous system (PNS) comprises the sensory organs that allow the fly to detect environmental factors such as temperature and pressure. PNS development is a highly specified process where each sensilla originates from a single sensory organ precursor (SOP) cell. One of the major genetic orchestrators of PNS development is Senseless, which encodes a zinc finger transcription factor (Sens). Sens is both necessary and sufficient for SOP differentiation. Senseless expression and SOP number are regulated by the microRNA miR-9a. However, the reciprocal dynamics of Senseless and miR-9a are still obscure. By coupling single-molecule FISH with immunofluorescence, we are able to visualize transcription of the mir-9a locus and expression of Sens simultaneously. During embryogenesis, we show that the expression of mir-9a in SOP cells is rapidly lost as Senseless expression increases. However, this mutually exclusive expression pattern is not observed in the third instar imaginal wing disc, where some Senseless-expressing cells show active sites of mir-9a transcription. These data challenge and extend previous models of Senseless regulation and show complex co-expression dynamics between mir-9a and Senseless. The differences in this dynamic relationship between embryonic and larval PNS development suggest a possible switch in miR-9a function. Our work brings single-cell resolution to the understanding of dynamic regulation of PNS development by Senseless and miR-9a.

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Wei, Nan, Lizhou Wang, Min Xu, Tianzhi An, Xueqing Huang, and Shi Zhou. "Research on mechanism of tanshinone a in regulating biological characteristics of hematopoietic stem cell in liver cirrhosis through targeting of miR-9a-5p." Materials Express 12, no. 5 (May 1, 2022): 653–59. http://dx.doi.org/10.1166/mex.2022.2194.

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This study assessed the mechanism of tanshinone A in regulating biological characteristics of Hematopoietic Stem Cell (HSC) in liver cirrhosis through targeting of miR-9a-5p. HSC cells were divided into negative control group and stimulated miR-9a-5p inhibitor group. Transfection was performed according to specification of the kit. Expression of miR-9a-5p was assessed with Real-time polymerase chain reaction (PCR). Cell proliferation was tested with flow cytometry (FCM), and α-smooth muscle actin (SMA) and Type I collagen expressions were detected with Western Blot assay. Caspase-3 activity was tested with spectrophotometry, while variation of inflammatory factor was detected with enzyme-linked immunosorbent assay (ELISA). There was higher miR-9a-5p level in HSC induced by Chemokine (C-C motif) ligands 4 (CCL-4). Biological characteristics of HSC induced by CCL-4 was restrained by down-regulation of miR-9a-5p, and presentation quantity of α-SMA and Type I collagen was reduced. So, occurrence of inflammation and migration of HSC could be restrained. The presentation quantity of Type I collagen was reduced with tanshinone A, and expression of miR-9a-5p was reduced. HSC characteristics in liver cirrhosis were affected by tanshinone A probably through regulating miR-9a-5p. It could provide a brand-new selection for treatment on liver cirrhosis.

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Li, Shan-Shan, Yang Wu, Xin Jin, and Chun Jiang. "The SUR2B subunit of rat vascular KATP channel is targeted by miR-9a-3p induced by prolonged exposure to methylglyoxal." American Journal of Physiology-Cell Physiology 308, no. 2 (January 15, 2015): C139—C145. http://dx.doi.org/10.1152/ajpcell.00311.2014.

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ATP-sensitive K+ (KATP) channels regulate plasma membrane excitability. The Kir6.1/SUR2B isoform of KATP channels is expressed in vascular smooth muscles and plays an important role in vascular tone regulation. This KATP channel is targeted by several reactive species. One of them is methylglyoxal (MGO), which is overly produced with persistent hyperglycemia and contributes to diabetic vascular complications. We have previously found that MGO causes posttranscriptional inhibition of the KATP channel, aggravating vascular tone regulation. Here we show evidence for the underlying molecular mechanisms. We screened microRNA databases and found several candidates. Of them, miR-9a-3p, increased its expression level by ∼240% when the cultured smooth muscle cell line was exposed to micromolar concentrations of MGO. Treatments with exogenous miR-9a-3p downregulated the SUR2B but not Kir6.1 mRNA. Antisense nucleotides of miR-9a-3p alleviated the effects of MGO. Quantitative PCR showed that the targeting sites of the miR-9a-3p were likely to be in the coding region of SUR2B. The effects of miR-9a-3p were mostly eliminated when the potential targeting site in SUR2B was site-specifically mutated. Our functional assays showed that KATP currents were impaired by miR-9a-3p induced with MGO treatment. These results suggest that MGO exposure raises the expression of miR-9a-3p, which subsequently downregulates the SUR2B mRNA, compromising KATP channel function in vascular smooth muscle.

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Ma, Chunli, Qing Gao, Li Zhang, Geng Wu, Chao Li, Jun Chen, Yuxuan Fu, and Lei Yang. "miR-9a-5p Protects Ischemic Stroke by Regulating Oxidative Stress and Mitochondrial Autophagy." Disease Markers 2023 (February 17, 2023): 1–9. http://dx.doi.org/10.1155/2023/5146305.

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Purpose. Present research is aimed at exploring the effect of miR-9a-5p on mitochondrial autophagy and alleviating cellular oxidative stress injury in ischemic stroke. Methods. SH-SY5Y cells were cultured with oxygen-glucose deprivation/reoxygenation (OGD/R) to simulate ischemia/reperfusion. The cells were treated in an anaerobic incubator (95% N2, 5% CO2) for 2 h and then reoxygenated in the normoxic condition for 24 h with 2 ml of normal medium. Cells were transfected with miR-9a-5p mimic/inhibitor or negative control. The RT-qPCR assay was utilized to measure the mRNA expression. Western blot was utilized to evaluate the protein expression. The CCK-8 assay was conducted to detect cell viability. Flow cytometry was applied to examine apoptosis and the cell cycle. The ELISA assay was applied to measure the contents of SOD and MDA in mitochondria. Autophagosomes were observed via electron microscopy. Results. By comparison with the control group, the miR-9a-5p expression in the OGD/R group obviously declined. Mitochondrial crista breaks, vacuole-like changes, and increased autophagosome formation were observed in the OGD/R group. OGD/R injury enhanced oxidative stress damage and mitophagy. When transfected with the miR-9a-5p mimic, mitophagosome production of SH-SY5Y cells decreased and oxidative stress injury was inhibited. However, the miR-9a-5p inhibitor obviously increased mitophagosome production and enhanced oxidative stress injury. Conclusion. miR-9a-5p protects against ischemic stroke by inhibiting OGD/R-induced mitochondrial autophagy and alleviating cellular oxidative stress injury.

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Das Gupta, Shalini, Robert Ciszek, Mette Heiskanen, Niina Lapinlampi, Janne Kukkonen, Ville Leinonen, Noora Puhakka, and Asla Pitkänen. "Plasma miR-9-3p and miR-136-3p as Potential Novel Diagnostic Biomarkers for Experimental and Human Mild Traumatic Brain Injury." International Journal of Molecular Sciences 22, no. 4 (February 4, 2021): 1563. http://dx.doi.org/10.3390/ijms22041563.

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Noninvasive, affordable circulating biomarkers for difficult-to-diagnose mild traumatic brain injury (mTBI) are an unmet medical need. Although blood microRNA (miRNA) levels are reportedly altered after traumatic brain injury (TBI), their diagnostic potential for mTBI remains inconclusive. We hypothesized that acutely altered plasma miRNAs could serve as diagnostic biomarkers both in the lateral fluid percussion injury (FPI) model and clinical mTBI. We performed plasma small RNA-sequencing from adult male Sprague–Dawley rats (n = 31) at 2 days post-TBI, followed by polymerase chain reaction (PCR)-based validation of selected candidates. miR-9a-3p, miR-136-3p, and miR-434-3p were identified as the most promising candidates at 2 days after lateral FPI. Digital droplet PCR (ddPCR) revealed 4.2-, 2.8-, and 4.6-fold elevations in miR-9a-3p, miR-136-3p, and miR-434-3p levels (p < 0.01 for all), respectively, distinguishing rats with mTBI from naïve rats with 100% sensitivity and specificity. DdPCR further identified a subpopulation of mTBI patients with plasma miR-9-3p (n = 7/15) and miR-136-3p (n = 5/15) levels higher than one standard deviation above the control mean at <2 days postinjury. In sTBI patients, plasma miR-9-3p levels were 6.5- and 9.2-fold in comparison to the mTBI and control groups, respectively. Thus, plasma miR-9-3p and miR-136-3p were identified as promising biomarker candidates for mTBI requiring further evaluation in a larger patient population.

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Song, Fei, Yong Huang, Xin Wang, Shunming Tang, and Xingjia Shen. "Bmo-miR-9a down regulates the expression ofBm-aseGenein vitro." Биоорганическая химия 39, no. 2 (2013): 194–99. http://dx.doi.org/10.7868/s013234231302005x.

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Cassidy, Justin J., Alexander J. Straughan, and Richard W. Carthew. "Differential Masking of Natural Genetic Variation by miR-9a in Drosophila." Genetics 202, no. 2 (November 27, 2015): 675–87. http://dx.doi.org/10.1534/genetics.115.183822.

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9

Bejarano, Fernando, Peter Smibert, and Eric C. Lai. "miR-9a prevents apoptosis during wing development by repressing Drosophila LIM-only." Developmental Biology 338, no. 1 (February 2010): 63–73. http://dx.doi.org/10.1016/j.ydbio.2009.11.025.

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Yatsenko, Andriy S., and Halyna R. Shcherbata. "Drosophila miR-9a Targets the ECM Receptor Dystroglycan to Canalize Myotendinous Junction Formation." Developmental Cell 28, no. 3 (February 2014): 335–48. http://dx.doi.org/10.1016/j.devcel.2014.01.004.

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Song, Fei, Yong Huang, Xin Wang, Shunming Tang, and Xingjia Shen. "Bmo-miR-9a down regulates the expression of Bm-ase Gene in vitro." Russian Journal of Bioorganic Chemistry 39, no. 2 (March 2013): 170–75. http://dx.doi.org/10.1134/s1068162013020052.

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12

Chen, Fengshou, Jie Han, Xiaoqian Li, Zaili Zhang, and Dan Wang. "Identification of the biological function of miR-9 in spinal cord ischemia-reperfusion injury in rats." PeerJ 9 (May 13, 2021): e11440. http://dx.doi.org/10.7717/peerj.11440.

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Spinal cord ischemia–reperfusion injury (SCII) is still a serious problem, and the mechanism is not fully elaborated. In the rat SCII model, qRT-PCR was applied to explore the altered expression of miR-9 (miR-9a-5p) after SCII. The biological function of miR-9 and its potential target genes based on bioinformatics analysis and experiment validation in SCII were explored next. Before the surgical procedure of SCII, miR-9 mimic and inhibitor were intrathecally infused. miR-9 mimic improved neurological function. In addition, miR-9 mimic reduced blood-spinal cord barrier (BSCB) disruption, inhibited apoptosis and decreased the expression of IL-6 and IL-1β after SCII. Gene Ontology (GO) analysis demonstrated that the potential target genes of miR-9 were notably enriched in several biological processes, such as “central nervous system development”, “regulation of growth” and “response to cytokine”. The Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed that the potential target genes of miR-9 were significantly enriched in several signaling pathways, including “Notch signaling pathway”, “MAPK signaling pathway”, “Focal adhesion” and “Prolactin signaling pathway”. We further found that the protein expression of MAP2K3 and Notch2 were upregulated after SCII while miR-9 mimic reduced the increase of MAP2K3 and Notch2 protein. miR-9 mimic or MAP2K3 inhibitor reduced the release of IL-6 and IL-1β. miR-9 mimic or si-Notch2 reduced the increase of cleaved-caspase3. Moreover, MAP2K3 inhibitor and si-Notch2 reversed the effects of miR-9 inhibitor. In conclusion, overexpression of miR-9 improves neurological outcomes after SCII and might inhibit BSCB disruption, neuroinflammation, and apoptosis through MAP2K3-, or Notch2-mediated signaling pathway in SCII.

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Nie, Cuifang, Guangju Meng, Yongyun Wu, Li Liu, Li Chen, Shengqiang Yang, and Yan Hu. "Expression of miR-9a-5p in cirrhosis patients with recurrent portal hypertension after treatment." Advances in Clinical and Experimental Medicine 30, no. 8 (August 18, 2021): 789–95. http://dx.doi.org/10.17219/acem/135980.

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Cassidy, Justin J., Aashish R. Jha, Diana M. Posadas, Ritika Giri, Koen J. T. Venken, Jingran Ji, Hongmei Jiang, Hugo J. Bellen, Kevin P. White, and Richard W. Carthew. "miR-9a Minimizes the Phenotypic Impact of Genomic Diversity by Buffering a Transcription Factor." Cell 155, no. 7 (December 2013): 1556–67. http://dx.doi.org/10.1016/j.cell.2013.10.057.

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Cassidy, Justin J., Aashish R. Jha, Diana M. Posadas, Ritika Giri, Koen J. T. Venken, Jingran Ji, Hongmei Jiang, Hugo J. Bellen, Kevin P. White, and Richard W. Carthew. "miR-9a Minimizes the Phenotypic Impact of Genomic Diversity by Buffering a Transcription Factor." Cell 157, no. 3 (April 2014): 753. http://dx.doi.org/10.1016/j.cell.2014.04.003.

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Li, Chengjun, Wei Wu, Jing Tang, Fan Feng, Peng Chen, and Bin Li. "Identification and Characterization of Development-Related microRNAs in the Red Flour Beetle, Tribolium castaneum." International Journal of Molecular Sciences 24, no. 7 (April 3, 2023): 6685. http://dx.doi.org/10.3390/ijms24076685.

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MicroRNAs (miRNAs) play important roles in insect growth and development, but they were poorly studied in insects. In this study, a total of 883 miRNAs were detected from the early embryo (EE), late larva (LL), early pupa (EP), late pupa (LP), and early adult (EA) of Tribolium castaneum by microarray assay. Further analysis identified 179 differentially expressed unique miRNAs (DEmiRNAs) during these developmental stages. Of the DEmiRNAs, 102 DEmiRNAs exhibited stage-specific expression patterns during development, including 53 specifically highly expressed miRNAs and 20 lowly expressed miRNAs in EE, 19 highly expressed miRNAs in LL, 5 weakly expressed miRNAs in EP, and 5 abundantly expressed miRNAs in EA. These miRNAs were predicted to target 747, 265, 472, 234, and 121 genes, respectively. GO enrichment analysis indicates that the targets were enriched by protein phosphorylation, calcium ion binding, sequence-specific DNA binding transcription factor activity, and cytoplasm. An RNA interference-mediated knockdown of the DEmiRNAs tca-miR-6-3p, tca-miR-9a-3p, tca-miR-9d-3p, tca-miR-11-3p, and tca-miR-13a-3p led to defects in metamorphosis and wing development of T. castaneum. This study has completed the identification and characterization of development-related miRNAs in T. castaneum, and will enable us to investigate their roles in the growth and development of insect.

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Huang, Songqian, Yuki Ichikawa, Kazutoshi Yoshitake, Shigeharu Kinoshita, Yoji Igarashi, Fumito Omori, Kaoru Maeyama, Kiyohito Nagai, Shugo Watabe, and Shuichi Asakawa. "Identification and Characterization of microRNAs and Their Predicted Functions in Biomineralization in the Pearl Oyster (Pinctada fucata)." Biology 8, no. 2 (June 17, 2019): 47. http://dx.doi.org/10.3390/biology8020047.

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The biological process of pearl formation is an ongoing research topic, and a number of genes associated with this process have been identified. However, the involvement of microRNAs (miRNAs) in biomineralization in the pearl oyster, Pinctada fucata, is not well understood. In order to investigate the divergence and function of miRNAs in P. fucata, we performed a transcriptome analysis of small RNA libraries prepared from adductor muscle, gill, ovary, and mantle tissues. We identified 186 known and 42 novel miRNAs in these tissues. Clustering analysis showed that the expression patterns of miRNAs were similar among the somatic tissues, but they differed significantly between the somatic and ovary tissues. To validate the existence of the identified miRNAs, nine known and three novel miRNAs were verified by stem-loop qRT-PCR using U6 snRNA as an internal reference. The expression abundance and target prediction between miRNAs and biomineralization-related genes indicated that miR-1990c-3p, miR-876, miR-9a-3p, and novel-3 may be key factors in the regulatory network that act by controlling the formation of matrix proteins or the differentiation of mineralogenic cells during shell formation in mantle tissue. Our findings serve to further clarify the processes underlying biomineralization in P. fucata.

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Wang, Ni, Chao Zhang, Min Chen, Zheyi Shi, Ying Zhou, Xiaoxiao Shi, Wenwu Zhou, and Zengrong Zhu. "Characterization of MicroRNAs Associated with Reproduction in the Brown Planthopper, Nilaparvata lugens." International Journal of Molecular Sciences 23, no. 14 (July 15, 2022): 7808. http://dx.doi.org/10.3390/ijms23147808.

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Insects have a robust capacity to produce offspring for propagation, and the reproductive events of female insects have been achieved at the molecular and physiological levels via regulatory gene pathways. However, the roles of MicroRNAs (miRNAs) in the reproductive development of the brown planthopper (BPH), Nilaparvata lugens, remain largely unexplored. To understand the roles of miRNAs in reproductive development, miRNAs were identified by Solexa sequencing in short-winged (SW) female adults of BPH. Small RNA libraries derived from three developmental phases (1 day, 3 days, and 5 days after emergence) were constructed and sequenced. We identified 905 miRNAs, including 263 known and 642 novel miRNAs. Among them, a total of 43 miRNAs were differentially expressed in the three developmental phases, and 14,568 putative targets for 43 differentially expressed miRNAs (DEMs) were predicted by TargetScan and miRanda. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis of the predicted miRNA targets illustrated the putative roles for these DEMs in reproduction. The progress events were annotated, including oogenesis, lipid biosynthetic process, and related pathways such as apoptosis, ABC transporters, and amino acid metabolism. Four highly abundant DEMs (miR-9a-5p, miR-34-5p, miR-275-3p, and miR-317-3p) were further screened, and miR-34-5p was confirmed to be involved in the regulation of reproduction. Overexpression of miR-34-5p via injecting its mimics reduced fecundity and decreased Vg expression. Moreover, target genes prediction for miR-34-5p showed they might be involved in 20E signaling cascades, apoptosis, and gonadal development, including hormone receptor 4 (HR4), caspase-1 (Cp-1), and spermatogenesis-associated protein 20 (SPATA20). These findings provide a valuable resource for future studies on the role of miRNAs in BPH reproductive development.

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Daniel, Scott G., Atlantis D. Russ, Kathryn M. Guthridge, Ammad I. Raina, Patricia S. Estes, Linda M. Parsons, Helena E. Richardson, Joyce A. Schroeder, and Daniela C. Zarnescu. "miR-9a mediates the role of Lethal giant larvae as an epithelial growth inhibitor in Drosophila." Biology Open 7, no. 1 (December 20, 2017): bio027391. http://dx.doi.org/10.1242/bio.027391.

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Biryukova, Inna, Joëlle Asmar, Houari Abdesselem, and Pascal Heitzler. "Drosophila mir-9a regulates wing development via fine-tuning expression of the LIM only factor, dLMO." Developmental Biology 327, no. 2 (March 2009): 487–96. http://dx.doi.org/10.1016/j.ydbio.2008.12.036.

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Qi, Feng. "MiR-9a-5p regulates proliferation and migration of hepatic stellate cells under pressure through inhibition of Sirt1." World Journal of Gastroenterology 21, no. 34 (2015): 9900. http://dx.doi.org/10.3748/wjg.v21.i34.9900.

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Heiskanen, Mette, Shalini Das Gupta, James D. Mills, Erwin A. van Vliet, Eppu Manninen, Robert Ciszek, Pedro Andrade, Noora Puhakka, Eleonora Aronica, and Asla Pitkänen. "Discovery and Validation of Circulating microRNAs as Biomarkers for Epileptogenesis after Experimental Traumatic Brain Injury–The EPITARGET Cohort." International Journal of Molecular Sciences 24, no. 3 (February 1, 2023): 2823. http://dx.doi.org/10.3390/ijms24032823.

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Traumatic brain injury (TBI) causes 10–20% of structural epilepsies and 5% of all epilepsies. The lack of prognostic biomarkers for post-traumatic epilepsy (PTE) is a major obstacle to the development of anti-epileptogenic treatments. Previous studies revealed TBI-induced alterations in blood microRNA (miRNA) levels, and patients with epilepsy exhibit dysregulation of blood miRNAs. We hypothesized that acutely altered plasma miRNAs could serve as prognostic biomarkers for brain damage severity and the development of PTE. To investigate this, epileptogenesis was induced in adult male Sprague Dawley rats by lateral fluid-percussion-induced TBI. Epilepsy was defined as the occurrence of at least one unprovoked seizure during continuous 1-month video-electroencephalography monitoring in the sixth post-TBI month. Cortical pathology was analyzed by magnetic resonance imaging on day 2 (D2), D7, and D21, and by histology 6 months post-TBI. Small RNA sequencing was performed from tail-vein plasma samples on D2 and D9 after TBI (n = 16, 7 with and 9 without epilepsy) or sham operation (n = 4). The most promising miRNA biomarker candidates were validated by droplet digital polymerase chain reaction in a validation cohort of 115 rats (8 naïve, 17 sham, and 90 TBI rats [21 with epilepsy]). These included 7 brain-enriched plasma miRNAs (miR-434-3p, miR-9a-3p, miR-136-3p, miR-323-3p, miR-124-3p, miR-212-3p, and miR-132-3p) that were upregulated on D2 post-TBI (p < 0.001 for all compared with naïve rats). The acute post-TBI plasma miRNA profile did not predict the subsequent development of PTE or PTE severity. Plasma miRNA levels, however, predicted the cortical pathology severity on D2 (Spearman ρ = 0.345–0.582, p < 0.001), D9 (ρ = 0.287–0.522, p < 0.001–0.01), D21 (ρ = 0.269–0.581, p < 0.001–0.05) and at 6 months post-TBI (ρ = 0.230–0.433, p < 0.001–0.05). We found that the levels of 6 of 7 miRNAs also reflected mild brain injury caused by the craniotomy during sham operation (ROC AUC 0.76–0.96, p < 0.001–0.05). In conclusion, our findings revealed that increased levels of neuronally enriched miRNAs in the blood circulation after TBI reflect the extent of cortical injury in the brain but do not predict PTE development.

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Xu, Le, Jiao Zhang, Anran Zhan, Yaqin Wang, Xingzhou Ma, Wencai Jie, Zhenghong Cao, Mohamed A. A. Omar, Kang He, and Fei Li. "Identification and Analysis of MicroRNAs Associated with Wing Polyphenism in the Brown Planthopper, Nilaparvata lugens." International Journal of Molecular Sciences 21, no. 24 (December 21, 2020): 9754. http://dx.doi.org/10.3390/ijms21249754.

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Many insects are capable of developing two types of wings (i.e., wing polyphenism) to adapt to various environments. Though the roles of microRNAs (miRNAs) in regulating animal growth and development have been well studied, their potential roles in modulating wing polyphenism remain largely elusive. To identify wing polyphenism-related miRNAs, we isolated small RNAs from 1st to 5th instar nymphs of long-wing (LW) and short-wing (SW) strains of the brown planthopper (BPH), Nilaparvata lugens. Small RNA libraries were then constructed and sequenced, yielding 158 conserved and 96 novel miRNAs. Among these, 122 miRNAs were differentially expressed between the two BPH strains. Specifically, 47, 2, 27 and 41 miRNAs were more highly expressed in the 1st, 3rd, 4th and 5th instars, respectively, of the LW strain compared with the SW strain. In contrast, 47, 3, 29 and 25 miRNAs were more highly expressed in the 1st, 3rd, 4th and 5th instars, respectively, of the SW strain compared with the LW strain. Next, we predicted the targets of these miRNAs and carried out Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis. We found that a number of pathways might be involved in wing form determination, such as the insulin, MAPK, mTOR, FoxO and thyroid hormone signaling pathways and the thyroid hormone synthesis pathway. Thirty and 45 differentially expressed miRNAs targeted genes in the insulin signaling and insect hormone biosynthesis pathways, respectively, which are related to wing dimorphism. Among these miRNAs, Nlu-miR-14-3p, Nlu-miR-9a-5p and Nlu-miR-315-5p, were confirmed to interact with insulin receptors (NlInRs) in dual luciferase reporter assays. These discoveries are helpful for understanding the miRNA-mediated regulatory mechanism of wing polyphenism in BPHs and shed new light on how insects respond to environmental cues through developmental plasticity.

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Gao, Yonghui, Lu Yang, Yulan Chen, Peiwen Liu, Ying Zhou, Xiaoguang Chen, and Jinbao Gu. "Aal-circRNA-407 regulates ovarian development of Aedes albopictus, a major arbovirus vector, via the miR-9a-5p/Foxl axis." PLOS Pathogens 19, no. 5 (May 5, 2023): e1011374. http://dx.doi.org/10.1371/journal.ppat.1011374.

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Aedes albopictus shows a rapid global expansion and dramatic vectorial capacity for various arboviruses, thus posing a severe threat to global health. Although many noncoding RNAs have been confirmed to play functional roles in various biological processes in Ae. albopictus, the roles of circRNA remain a mystery. In the present study, we first performed high-throughput circRNA sequencing in Ae. albopictus. Then, we identified a cysteine desulfurase (CsdA) superfamily gene-originated circRNA, named aal-circRNA-407, which was the third most abundant circRNA in adult females and displayed a fat body highly expressed manifestation and blood feeding-dependent onset. SiRNA-mediated knockdown of circRNA-407 resulted in a decrease in the number of developing follicles and a reduction in follicle size post blood meal. Furthermore, we demonstrated that circRNA-407 can act as a sponge of aal-miR-9a-5p to promote the expression of its target gene Foxl and eventually regulate ovarian development. Our study is the first to report a functional circRNA in mosquitoes, expanding our current understanding of important biological roles in mosquitoes and providing an alternative genetic strategy for mosquito control.

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Biryukova, Inna, Joëlle Asmar, Claudine Ackermann, Nadine Arbogast, and Pascal Heitzler. "01-P016 The Drosophila LIM-only, dLMO transcription factor that controls sensory organ and wing developments, is regulated by mir-9a." Mechanisms of Development 126 (August 2009): S55—S56. http://dx.doi.org/10.1016/j.mod.2009.06.017.

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He, Shuang, Zongyu Chen, Chunju Xue, Leilei Zhou, Chunyu Li, Wenqing Jiang, Siyu Lian, Yi Shen, Minghua Liao, and Xianming Zhang. "MiR-9a-5p alleviates ventilator-induced lung injury in rats by inhibiting the activation of the MAPK signaling pathway via CXCR4 expression downregulation." International Immunopharmacology 112 (November 2022): 109288. http://dx.doi.org/10.1016/j.intimp.2022.109288.

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Fishov, Hila, Eli Muchtar, Mali Salmon-Divon, Angela Dispenzieri, Ofer Shpilberg, and Oshrat Rokah. "The Role of Non-Coding RNAs in the Pathogenesis of AL Amyloidosis." Blood 138, Supplement 1 (November 5, 2021): 2659. http://dx.doi.org/10.1182/blood-2021-150828.

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Abstract Background: Systemic light chain (AL) amyloidosis is a clonal plasma cell disorder characterized by deposition of misfolded immunoglobulin light chain products in vital organs, causing their dysfunction. All therapies used to treat AL patients are adapted from multiple myeloma (MM) and customized to the typically frail AL population. Hence, it is important to identify novel therapeutic targets for these patients. MicroRNAs (miRNAs) are short, non-coding RNAs that regulate gene expression and have a role in cancer development and progression. MiRNAs can be purified from serum, plasma and bone marrow (BM) and may be used as biomarkers to distinguish between patients and healthy individuals. Moreover, miRNA-mRNA interactions may determine the molecular mechanism involved in AL pathogenesis and may suggest novel therapeutic approaches. To date, knowledge about circulating or BM miRNAs involved in AL amyloidosis is lacking. Aims: To decipher specific miRNA expression profiles in AL amyloidosis compared to MM patients and healthy controls (HC) and to examine how miRNAs are involved in AL pathogenesis. Methods: miRNA expression profile was determined using the nCounter assay (NanoString technologies). RNA-Seq data was downloaded from GEO database (GSE175384), and was used to detect potential miRNA-mRNA targets, and enriched biological pathways by the bioinformatics tool Ingunity Pathway Analysis (IPA). MiRNA and gene expression profiles were validated by qRT-PCR in 60 AL, 60 MM and 10 HC samples. The effect of aberrantly expressed miRNAs on potential molecular targets was analyzed in ALMC1 cells by transfecting the cells with miRNA mimic, following qRT-PCR, Western blot analysis and Annexin-PI staining. Results: BM and plasma miRNAs were differentially expressed in AL amyloidosis compared to MM or HC. MiRs-9a-5p, 181a-5p, 199a-3p, 130a-3p, 145-5p and 301a-3p were differentially expressed between AL and MM samples and may be used as biomarkers for distinguish AL amyloidosis from MM. Moreover, we found that the differentially expressed miRNAs and mRNA in AL patients regulates key signaling pathways related to cell cycle and anti-apoptosis mechanisms including cytokine signaling, oxidative phosphorylation (OXPHOS), NFkB signaling, activation of MAPK and PI3K/AKT pathways, which are all linked to cancer cell growth, proliferation and therapeutic resistance, and therefore may be used as a therapeutic targets. Specifically, our analysis showed that genes related to mitochondrial activity were upregulated in AL patients (Figure 1), particularly the anti-apoptotic BCL2 family genes (BCL2, MCL1, and BCL2L1). MCL1 and BCL2L1 are predicted targets of miR-181a-5p that was downregulated in BM and plasma samples of AL patients compared to MM patients, indicating a possible interaction between these molecules. MiR-9-5p, which was also found to be downregulated in AL BM and plasma samples compared to MM patients, is predicted to have an indirect effect on the BCL2 family members through CREB molecule (Figure 1). The biological significance of miR-9-5p and miR-181a-5p was evaluated, by transfecting ALMC1 cell line with miRNA mimics. Overexpression of these miRNAs led to downregulation of the BCL2 family anti-apoptotic genes and induced apoptosis by Annexin V staining. These findings might explain the biological mechanism by which AL patients respond to the BCL2 inhibitor, venetoclax, as recently reported (Sidiqi et al, BCJ, 2020). Conclusions: We provide insight into the molecular mechanisms mediated by miRNAs and the aberrant expression of oncogenic/tumor suppressor genes. The differential expression of miRNAs in AL amyloidosis may be used to understand disease pathogenesis and predict risk of progression to AL amyloidosis among patients with known plasma cell disorders. Additionally, signaling pathways involved in AL amyloidosis, mediated by miRNAs, may assist in tailoring more specific treatments. Figure 1 Figure 1. Disclosures Dispenzieri: Oncopeptides: Consultancy; Sorrento Therapeutics: Consultancy; Pfizer: Research Funding; Alnylam: Research Funding; Takeda: Research Funding; Janssen: Consultancy, Research Funding.

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Gallicchio, Lorenzo, Sam Griffiths-Jones, and Matthew Ronshaugen. "miR-9a regulates levels of both rhomboid mRNA and protein in the early Drosophila melanogaster embryo." G3 Genes|Genomes|Genetics 12, no. 4 (February 10, 2022). http://dx.doi.org/10.1093/g3journal/jkac026.

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Abstract MicroRNAs can have subtle and combinatorial effects on the levels of the targets and pathways they act on. Studying the consequences of a single microRNA knockout often proves difficult as many such knockouts exhibit phenotypes only under stress conditions. This has often led to the hypothesis that microRNAs buffer the effects of intrinsic and environmental stochasticity on gene expression. Observing and understanding this buffering effect entails quantitative analysis of microRNA and target expression in single cells. To this end, we have employed single-molecule fluorescence in situ hybridization, immunofluorescence, and high-resolution confocal microscopy to investigate the effects of miR-9a loss on the expression of the serine-protease Rhomboid in Drosophila melanogaster early embryos. Our single-cell quantitative approach shows that spatially, the rhomboid mRNA pattern is identical in WT and miR-9a knockout embryos. However, we find that the number of mRNA molecules per cell is higher when miR-9a is absent, and the level and temporal accumulation of rhomboid protein shows a more dramatic increase in the miR-9a knockout. Specifically, we see accumulation of rhomboid protein in miR-9a mutants by stage 5, much earlier than in WT. The data, therefore, show that miR-9a functions in the regulation of rhomboid mRNA and protein levels. While further work is required to establish whether rhomboid is a direct target of miR-9 in Drosophila, our results further establish the miR-9 family microRNAs as conserved regulators of timing in neurogenic processes. This study shows the power of single-cell quantification as an experimental tool to study phenotypic consequences of microRNA mis-regulation.

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Curty-Costa, Ernesto, Luísa Hoffmann, Rosane Silva, Turán P. Ürményi, and Debora S. Faffe. "Abstract 41: Different MicroRNA Expression Profiles in Murine Aorta and Carotid Arteries." Circulation Research 117, suppl_1 (July 17, 2015). http://dx.doi.org/10.1161/res.117.suppl_1.41.

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Atherosclerosis, a major cause of death, affects vascular walls diffusely. Some vascular beds are, however, preferentially involved. Small noncoding RNAs, microRNAs, have emerged as key regulators of gene expression in either physiological or pathophysiological processes. Here, we investigated whether different vascular beds, commonly affected by atherosclerosis, present specific microRNA expression profiles. To this end, aorta (Ao) and carotid (Ca) arteries from two male Wistar rats (200 g) were dissected, total RNA was extracted with Trizol, and the small RNA fraction was enriched using magnetic beads. Sequencing was performed using RNA-Seq on Ion Torrent PGM platform and data were analyzed using CLC Genomics Workbench software. We identified 372 and 305 microRNAs in Ca and Ao, respectively - the arteries shared 280 microRNAs. The majority of the 20 most expressed microRNAs were similar between the arteries. Of these top 20, 90% in the Ao were also among the most expressed in Ca, and in Ca 65% were also among the most expressed in Ao. Both mechano and platelet-microRNAs were identified in both arteries. Note that overexpression of mechano-miR-21 is reported to attenuate lipid accumulation and to reduce inflammation, preventing atherosclerosis. We detected mechano-miR-21, however, only in the Ao. We also found that murine aorta and carotid arteries express differently 29 microRNAs (p<0.05). Among the 29 microRNAs, 8 (28%) have been related to atherosclerosis. Of these, 6 were more expressed in Ca (miR-181, miR-9a-1, miR-9a-2, miR-511, miR-146, miR-27), and 2 were more expressed in Ao (miR-144 and miR-322). Note that 3 of the 6 more expressed microRNAs in Ca are related to atherosclerosis, that is: miR-181 regulates cell stress and proliferation; miR-511 regulates cholesterol synthesis, and miR-27 is a known marker of the disease. Taken together, our results suggest that specific microRNA expression profiles may play a role in the vascular behavior during the atherosclerotic process.

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Yang, Di, Jie Yu, Hui-Bin Liu, Xiu-Qing Yan, Juan Hu, Yang Yu, Jing Guo, Ye Yuan, and Zhi-Min Du. "The long non-coding RNA TUG1-miR-9a-5p axis contributes to ischemic injuries by promoting cardiomyocyte apoptosis via targeting KLF5." Cell Death & Disease 10, no. 12 (December 2019). http://dx.doi.org/10.1038/s41419-019-2138-4.

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AbstractNon-coding RNAs participate in many cardiac pathophysiological processes, including myocardial infarction (MI). Here we showed the interplay between long non-coding RNA taurine-upregulated gene 1 (lncR-TUG1), miR-9a-5p (miR-9) and Krüppel-like factor 5 (KLF5). LncR-TUG1 was upregulated in ischemic heart and in cultured cardiomyocytes exposed to H2O2. Knockdown of lncR-TUG1 markedly ameliorated impaired cardiac function of MI mice. Further study showed that lncR-TUG1 acted as a competitive endogenous RNA of miR-9, and silencing of lncR-TUG1 inhibited cardiomyocyte apoptosis by upregulating miR-9 expression. Furthermore, the miR-9 overexpression obviously prevented ischemia injury and significantly inhibited H2O2-induced cardiomyocyte apoptosis via inhibition of mitochondrial apoptotic pathway. KLF5, as a target gene of miR-9 by dual-luciferase reporter assay, was involved in the process of miR-9 in regulating cardiomyocyte apoptosis. Our data identified the KLF5 was downregulated by miR-9 overexpression and knockdown of KLF5 inhibited cardiomyocyte apoptosis induced by H2O2. MiR-9 exerts anti-cardiomyocyte apoptotic affects by targeting KLF5. Collectively, our data identify a novel function of lncR-TUG1/miR-9/KLF5 axis in regulating cardiomyocyte apoptosis that affects myocardial infarction progression.

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Guo, Xiaojiao, Zongyuan Ma, Baozhen Du, Ting Li, Wudi Li, Lingling Xu, Jing He, and Le Kang. "Dop1 enhances conspecific olfactory attraction by inhibiting miR-9a maturation in locusts." Nature Communications 9, no. 1 (March 22, 2018). http://dx.doi.org/10.1038/s41467-018-03437-z.

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Li, Xiang, Mu‐Hua Zhao, Miao‐Miao Tian, Jing Zhao, Wan‐Lun Cai, and Hong‐Xia Hua. "An InR / mir‐9a / NlUbx regulatory cascade regulates wing diphenism in brown planthoppers." Insect Science, October 8, 2020. http://dx.doi.org/10.1111/1744-7917.12872.

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Bashiri, Hamideh, Maryam Moazam-Jazi, Mohammad Reza Karimzadeh, Saeideh Jafarinejad-Farsangi, Amirhossein Moslemizadeh, Marziyeh Lotfian, Zahra Miri Karam, Reza Kheirandish, and Mohammad Mojtaba Farazi. "Autophagy in combination therapy of temozolomide and IFN-γ in C6-induced glioblastoma: role of non-coding RNAs." Immunotherapy, August 16, 2023. http://dx.doi.org/10.2217/imt-2022-0212.

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Aim: We predicted the modulation of autophagy and apoptosis in response to temozolomide (TMZ) and IFN-γ based on changes in the expression of non-coding RNAs in C6-induced glioblastoma (GBM). Materials & methods: Each rat received an intraperitoneal injection of TMZ (7.5 mg/kg) and/or IFN-γ (50,000 IU). Results: The reduced expression of H19 and colorectal neoplasia differentially expressed ( CRNDE) was associated with a reduction in autophagy in response to TMZ, IFN-γ and TMZ + IFN-γ therapy, whereas the decreased level of miR-29a (proapoptotic miRNA) was associated with an increase in apoptosis. Conclusion: It appears that H19 promotes switching from autophagy to apoptosis in response to combination therapy of TMZ and IFN-γ through the miR-29a/autophagy-related protein 9A (ATG9A) pathway in C6-induced GBM.

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Colaianni, Davide, and Cristiano De Pittà. "The Role of microRNAs in the Drosophila Melanogaster Visual System." Frontiers in Cell and Developmental Biology 10 (April 4, 2022). http://dx.doi.org/10.3389/fcell.2022.889677.

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MicroRNAs (miRNAs) are a class of small non-coding RNAs (∼22 nucleotides in length) that negatively regulate protein-coding gene expression post-transcriptionally by targeting mRNAs and triggering either translational repression or RNA degradation. MiRNA genes represent approximately 1% of the genome of different species and it has been estimated that every miRNA can interact with an average of 200 mRNA transcripts, with peaks of 1,500 mRNA targets per miRNA molecule. As a result, miRNAs potentially play a fundamental role in several biological processes including development, metabolism, proliferation, and apoptotic cell death, both in physiological and pathological conditions. Since miRNAs were discovered, Drosophila melanogaster has been used as a model organism to shed light on their functions and their molecular mechanisms in the regulation of many biological and behavioral processes. In this review we focus on the roles of miRNAs in the fruit fly brain, at the level of the visual system that is composed by the compound eyes, each containing ∼800 independent unit eyes called ommatidia, and each ommatidium is composed of eight photoreceptor neurons that project into the optic lobes. We describe the roles of a set of miRNAs in the development and in the proper function of the optic lobes (bantam, miR-7, miR-8, miR-210) and of the compound eyes (bantam, miR-7, miR-9a, miR-210, miR-263a/b, miR-279/996), summarizing also the pleiotropic effects that some miRNAs exert on circadian behavior.

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Subramanian, Manivannan, Seung Jae Hyeon, Tanuza Das, Yoon Seok Suh, Yun Kyung Kim, Jeong-Soo Lee, Eun Joo Song, Hoon Ryu, and Kweon Yu. "UBE4B, a microRNA-9 target gene, promotes autophagy-mediated Tau degradation." Nature Communications 12, no. 1 (June 2, 2021). http://dx.doi.org/10.1038/s41467-021-23597-9.

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AbstractThe formation of hyperphosphorylated intracellular Tau tangles in the brain is a hallmark of Alzheimer’s disease (AD). Tau hyperphosphorylation destabilizes microtubules, promoting neurodegeneration in AD patients. To identify suppressors of tau-mediated AD, we perform a screen using a microRNA (miR) library in Drosophila and identify the miR-9 family as suppressors of human tau overexpression phenotypes. CG11070, a miR-9a target gene, and its mammalian orthologue UBE4B, an E3/E4 ubiquitin ligase, alleviate eye neurodegeneration, synaptic bouton defects, and crawling phenotypes in Drosophila human tau overexpression models. Total and phosphorylated Tau levels also decrease upon CG11070 or UBE4B overexpression. In mammalian neuroblastoma cells, overexpression of UBE4B and STUB1, which encodes the E3 ligase CHIP, increases the ubiquitination and degradation of Tau. In the Tau-BiFC mouse model, UBE4B and STUB1 overexpression also increase oligomeric Tau degradation. Inhibitor assays of the autophagy and proteasome systems reveal that the autophagy-lysosome system is the major pathway for Tau degradation in this context. These results demonstrate that UBE4B, a miR-9 target gene, promotes autophagy-mediated Tau degradation together with STUB1, and is thus an innovative therapeutic approach for AD.

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Epstein, Yehonatan, Noam Perry, Marina Volin, Maayan Zohar-Fux, Rachel Braun, Lilach Porat-Kuperstein, and Hila Toledano. "miR-9a modulates maintenance and ageing of Drosophila germline stem cells by limiting N-cadherin expression." Nature Communications 8, no. 1 (September 19, 2017). http://dx.doi.org/10.1038/s41467-017-00485-9.

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Zhang, Yi, Micheal Chopp, Xianshuang Liu, and Zheng Gang Zhang. "Abstract W P221: Argonaute 2 Mediates Sildenafil-Promoted Axonal Outgrowth." Stroke 45, suppl_1 (February 2014). http://dx.doi.org/10.1161/str.45.suppl_1.wp221.

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Molecular mechanisms are not fully known for the inhibitory effect of chondroitin sulfate proteoglycans (CSPGs) on axonal outgrowth. The present study investigated the effect of CSPGs on miRNA expression and the role of Argonaute 2 (Ago2) in mediating Sildenafil-induced axonal outgrowth under CSPG conditions. Primary rat embryonic cortical neurons were cultured in a microfluidic chamber which separates somata and axons. Selective application of CSPGs within the axonal compartment markedly inhibited axonal outgrowth (567±15 μm vs 688 ± 21 μm in control, n=5, p<0.05). Axonal application of Sildenafil, a PDE5 inhibitor, completely reversed the inhibitory effect of CSPG on axonal outgrowth (671±17 μm, n=5). Analysis of miRNA PCR array showed that axonal application of CSPGs robustly changed miRNA profiles not only in axons but also in somata, indicating that axonal signals regulate soma miRNAs. Sildenafil inversely altered miRNA up- and down-regulated by CSPGs, including miR-29c, miR-9a, miR-20b, miR-298 and miR-34a. Attenuation of Ago2, a regulator of miRNA activity, in neurons by siRNA abolished Sildenafil-increased axonal outgrowth under CSPG conditions, suggesting that miRNAs are required for Sildenafil-enhanced axonal outgrowth. One of putative targets of miR-29c is integrin β1. Western blot analysis showed that CSPGs and Sildenafil reduced and increased, respectively, axonal integrin β1 and its downstream protein, focal adhesion kinase, suggesting that miR-29c regulates these protein levels. To examine cause-effect of integrin β1, we applied a neutralizing antibody against integrin β1 into the axonal compartment and found that the antibody attenuated the Sildenafil-reversed inhibitor effect of CSPGs on axonal outgrowth (523±34 μm vs 671±17 μm in Sildenafil, n=5, p<0.01). In conclusion, the present study indicates that axonal signals induced by CSPGs and Sildenafil change miRNA profiles in the entire neuron and that Sildenafil abolishes the CSPG inhibitory effect on axons via Ago2.

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Suh, Yoon Seok, Shreelatha Bhat, Seung-Hyun Hong, Minjung Shin, Suhyoung Bahk, Kyung Sang Cho, Seung-Whan Kim, et al. "Genome-wide microRNA screening reveals that the evolutionary conserved miR-9a regulates body growth by targeting sNPFR1/NPYR." Nature Communications 6, no. 1 (July 3, 2015). http://dx.doi.org/10.1038/ncomms8693.

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Chmielewska, Natalia, Adriana Wawer, Zofia Wicik, Bartosz Osuch, Piotr Maciejak, and Janusz Szyndler. "miR-9a-5p expression is decreased in the hippocampus of rats resistant to lamotrigine: A behavioural, molecular and bioinformatics assessment." Neuropharmacology, January 2023, 109425. http://dx.doi.org/10.1016/j.neuropharm.2023.109425.

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Tu, Menjiang, Rui Wang, Pei Zhu, Qingqing Wang, Bishao Sun, Keshi Lu, Jiawei Zhang, et al. "Human Urine-Derived Stem Cells Improve Partial Bladder Outlet Obstruction in Rats: Preliminary Data and microRNA-mRNA Expression Profile." Stem Cell Reviews and Reports, March 1, 2022. http://dx.doi.org/10.1007/s12015-022-10340-0.

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AbstractPartial bladder outlet obstruction (pBOO) often results in bladder tissue inflammation and remodeling. As human urine-derived stem cells (USCs) have demonstrated therapeutic benefits, we used a rat model to investigate the effect of USCs on bladder function and explore the miRNA and gene expression profiles in bladder tissue using RNA sequencing. Eighteen rats were assigned to a sham surgery group, pBOO group, and pBOO+USC group (six biweekly treatments). Routine urodynamic monitoring, analysis of detrusor muscle strips, and pathophysiology assessments were conducted. Finally, altered miRNA and mRNA expression profiles of bladder tissue were examined using RNA sequencing and bioinformatics analysis. After USC treatment, elevated bladder compliance and maximal voiding pressure, declined end filling pressure and voided volume, and improved detrusor muscle contractility and carbachol sensitivity were found. Histology and TUNEL assay revealed reduced collagen deposition and muscle cell apoptosis in bladder tissue. The differential expression of eight miRNAs was reversed by USC treatment. Two large nodes (miR-142 and miR-9a) were identified in the miRNA-gene interaction network in the USC-treated group. The Kyoto Encyclopedia of Genes and Genomes analysis revealed enrichment of multiple significant pathways, including those involved in necroptosis and cytokine-cytokine receptor interactions. This is the first study to demonstrate the protective effect of USCs on bladder function and remodeling in pBOO rats. The miRNA and mRNA expression levels differed in the bladder of pBOO rats with and without USC treatment. Although the mechanism underlying these effects has not been fully elucidated, necroptosis and cytokine-cytokine receptor interaction-related pathways may be involved. Graphical abstract

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Gallicchio, Lorenzo, Sam Griffiths-Jones, and Matthew Ronshaugen. "Corrigendum to: Single-cell visualization of mir-9a and Senseless co-expression during Drosophila melanogaster embryonic and larval peripheral nervous system development." G3 Genes|Genomes|Genetics 11, no. 4 (April 1, 2021). http://dx.doi.org/10.1093/g3journal/jkab048.

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Chen, Xichen, Mao Mao, Ying Shen, Xueyong Jiang, and Zhifei Yin. "lncRNA TUG1 regulates human pulmonary microvascular endothelial cell apoptosis via sponging of the miR‑9a‑5p/BCL2L11 axis in chronic obstructive pulmonary disease." Experimental and Therapeutic Medicine 22, no. 2 (June 25, 2021). http://dx.doi.org/10.3892/etm.2021.10338.

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Journal articles on the topic 'MiR-9a'

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