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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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The effect of miR-294 and miR-181 on the transcriptome during OSK reprogramming of MEFs

ABSTRACT: Study designed to determine the immediate effects of supplementing OSK reprogramming with miR-294 or miR-181. MEFs were infected on day 0, and transfected with miR-294, miR-181 or control mimic on day 1. On day 3 RNA was extracted. OSK infected MEFs samples were compared to non-infected MEFs and to fully reprogrammed iPSCs. Performed in biological triplicate, with each sample containing different OSK viral stocks, different preparations of MEFs and independent transfections. Biological triplicate iPSCs represent three independent and clonally expanded iPSC lines. Total RNA collected with Trizol. All processing conducted at the UCLA Neuroscience Genomics Core. MouseRef-8 v2.0 Expression BeadChips.

ORGANISM(S): Mus musculus

SUBMITTER: Robert Blelloch

PROVIDER: E-GEOD-49556 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The effect of miR-294 and miR-181 on the transcriptome during OSK reprogramming of MEFs

Project description:Study designed to determine the immediate effects of supplementing OSK reprogramming with miR-294 or miR-181. MEFs were infected on day 0, and transfected with miR-294, miR-181 or control mimic on day 1. On day 3 RNA was extracted. OSK infected MEFs samples were compared to non-infected MEFs and to fully reprogrammed iPSCs.

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Expression analysis of OSK and Sall4+OSK reprogramming cells sorted for expression of miR-290 and/or miR-302.

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Expression analysis of OSK and Sall4+OSK reprogramming cells sorted for expression of miR-290 and/or miR-302.

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2014-03-31 | E-GEOD-54341 | biostudies-arrayexpress

Mus musculus

Project description:The effect of miR-294 and miR-181 on the transcriptome during OSK reprogramming of MEFs

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Project description:The intestinal epithelium is a key physical interface that integrates dietary and microbial signals to regulate nutrient uptake and mucosal homeostasis. Intestinal epithelial cells (IECs) have a high turnover rate driven by the death of terminally differentiated cells with concurrent stem cell proliferation, a process critical for maintaining intestinal homeostasis and protecting against mucosal inflammation. The transcriptional programs that regulate IEC quiescence, proliferation, and differentiation have been well-characterized. However, how gene expression networks critical for IEC functions are regulated at the post-transcriptional level during homeostasis or inflammatory disease remains poorly understood. Herein, we show that a conserved family of microRNAs, miR-181, is significantly downregulated in IECs from patients with inflammatory bowel disease and mice with chemical-induced colitis. Strikingly, we showed that miR-181 expression within IECs, but not the hematopoietic system, is required for protection against the development of severe colonic inflammation in response to epithelial injury in mice. Mechanistically, we showed that miR-181 expression increases the proliferative capacity of IECs, likely through the regulation of Wnt signaling, independently of gut microbiota composition. As epithelial reconstitution is crucial for restoring intestinal homeostasis after injury, the miR-181 family represents a potential novel therapeutic target in IECs for protection against severe intestinal inflammation.

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Global Transcriptional Analysis of Nuclear Reprogramming in the Transition from MEFs to iPSCs

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2012-10-01 | E-GEOD-37397 | biostudies-arrayexpress

Modulation of miR-181 influences dopaminergic neuronal degeneration in a mouse model of Parkinson’s disease

Project description:Parkinson’s disease (PD) is caused by loss of dopaminergic (DA) neurons in the substantia nigra (SN). Although PD pathogenesis is not fully understood, studies implicate perturbations in gene regulation, mitochondrial function, and neuronal activity. MicroRNAs (miRs) are small gene regulatory RNAs that inhibit diverse subsets of target mRNAs, and several studies have noted miR expression alterations in PD brains. For example, miR-181a is abundant in brain and is increased in PD patient brain samples; however, the disease relevance of this remains unclear. Herein, we show that miR-181 target mRNAs are broadly down-regulated in aging and PD brains. To address if the miR‑181 family plays a role in PD pathogenesis, we generated adeno-associated viruses (AAV) to overexpress and inhibit miR-181 isoforms. After co-injection with AAV overexpressing alpha-synuclein (aSyn) into mouse SN (PD model), we found that moderate miR-181a/b overexpression exacerbated aSyn-induced DA neuronal loss, whereas miR‑181 inhibition was neuroprotective, relative to controls (GFP-alone and/or scrambled RNA). Also, prolonged miR-181 overexpression in SN alone elicited measurable neurotoxicity coincident with an increased immune response. RNA-seq analyses revealed that miR-181a/b inhibits genes involved in synaptic transmission, neurite outgrowth, and mitochondrial respiration, along with several genes having known protective roles and genetic links in PD.

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