{"database":"biostudies-arrayexpress","file_versions":[],"scores":null,"additional":{"omics_type":["Metabolomics","Unknown","Transcriptomics","Genomics","Proteomics"],"submitter":["Li Genpeng"],"instrument_platform":["Illumina HiSeq 2000"],"study_type":["RNA-seq of non coding RNA"],"organism":["Homo sapiens"],"species":["Homo sapiens"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/E-MTAB-12659"],"description":["Hashimoto’s thyroiditis (HT) is an organ-specific autoimmune disease characterized by lymphocyte infiltration that destroys thyrocyte cells. To date, the underlying mechanisms responsible for these processes are incompletely understood. Here, we identified that miR-142-3p encapsulated in T lymphocyte-derived tissue small extracellular vesicle (sEV) can induce Treg function defect and thyrocyte destruction though an intact response loop, favoring the progression of HT. Inactivation of miR-142-3p can effectively protect NOD.H-2h4 mice from HT development which display reduced lymphocyte infiltration, lower antibody titer, and higher Treg cells. Looking at the mechanisms underlying sEV action on thyrocyte destruction, we found that the strong deleterious effect mediated by T lymphocyte-derived tissue sEV miR-142-3p is due to its ability to block the activation of the ERK1/2 signaling pathway through downregulating RAC1. Taken together, our findings highlight the fact that tissue sEV-mediated miR-142-3p transfer can serve as a communication mode between T lymphocytes and thyrocyte cells in HT."],"repository":["biostudies-arrayexpress"],"sample_protocol":["Library Construction - A total amount of 1ng-500ng RNA per sample was used as input material for the RNA sample preparations. Sequencing libraries were generated using QIAseq miRNA Library Kit (Qiagen, Frederick, MD) following manufacturer’s recommendations and index codes were added to attribute sequences to each sample.","Nucleic Acid Extraction - Total RNA from cell or tissue sEV was extracted using TRIzol reagent (Invitrogen) according to the manufacturer’s instructions. The RNA concentration was confirmed using absorbance measurements with a NanoDrop 2100 (Thermo Scientific).","Sequencing - Reverse transcription (RT) primers with unique molecular indices (UMIs) were introduced to analyze the quantification of miRNA expressions during cDNA synthesis and PCR amplification. At last, library quality was assessed on the Agilent Bioanalyzer 2100 and qPCR. The clustering of the index-coded samples was performed on  acBot Cluster Generation System using TruSeq PE Cluster Kitv3-cBot-HS (Illumina, San Diego, CA, USA) according to the manufacturer’s instructions. After cluster generation, the library preparations were sequenced on an Illumina Hiseq platform and paired-end  reads were generated.","Sample Collection - The thyroid tissue was very gently dissociated into small pieces and incubated with collagenase D and DNase I for 30 min at 37°C under mild agitation. Then, a filtration step with a 0.70 µm pore size filter is applied to remove the largest elements. The remaining liquid was differentially centrifuged at 300 × g for 10 min and 2,000 × g for 20 min to remove cells and tissue debris. The supernatant was then further centrifuged at 16,500 × g for 20 min and at 118,000 × g for 2.5 h to collect the sEV."],"figure_sub":["Organization","MINSEQE Score","Assays and Data","MAGE-TAB Files"],"pubmed_authors":["Li Genpeng"],"additional_accession":[]},"is_claimable":false,"name":"miR-142-3p encapsulated in T lymphocyte-derived tissue small extracellular vesicles induces Treg function defect and thyrocyte destruction in Hashimoto’s thyroiditis","description":"Hashimoto’s thyroiditis (HT) is an organ-specific autoimmune disease characterized by lymphocyte infiltration that destroys thyrocyte cells. To date, the underlying mechanisms responsible for these processes are incompletely understood. Here, we identified that miR-142-3p encapsulated in T lymphocyte-derived tissue small extracellular vesicle (sEV) can induce Treg function defect and thyrocyte destruction though an intact response loop, favoring the progression of HT. Inactivation of miR-142-3p can effectively protect NOD.H-2h4 mice from HT development which display reduced lymphocyte infiltration, lower antibody titer, and higher Treg cells. Looking at the mechanisms underlying sEV action on thyrocyte destruction, we found that the strong deleterious effect mediated by T lymphocyte-derived tissue sEV miR-142-3p is due to its ability to block the activation of the ERK1/2 signaling pathway through downregulating RAC1. Taken together, our findings highlight the fact that tissue sEV-mediated miR-142-3p transfer can serve as a communication mode between T lymphocytes and thyrocyte cells in HT.","dates":{"release":"2026-01-18T00:00:00Z","modification":"2026-01-18T02:02:23.231Z","creation":"2023-02-20T13:08:16.945Z"},"accession":"E-MTAB-12659","cross_references":{"ENA":["ERP145125"],"EFO":["EFO_0003737","EFO_0002944","EFO_0004170","EFO_0005518","EFO_0004184"]}}