<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE316nnn/GSE316801/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE316801</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>MiR-30d-5p modulation induces expression changes related to β-cell function, survival and regeneration</name><description>Type 1 diabetes is an autoimmune disease characterized by the destruction of insulin-producing β-cells, leading to hyperglycemia. A temporary partial remission (PR) phase often follows diagnosis, marked by improved glycemic control and reduced autoimmunity. This study investigates the role of miR-30d-5p, a microRNA highly expressed during PR, on beta-cell recovery and regeneration. Remarkably, human pancreatic slices were successfully transfected with oligonucleotides (miR-30d-5p inhibitor or mimic), enabling exploration of post-transcriptional regulation in a human context. Bulk RNA sequencing on human pancreatic slices from 3 non-diabetic donors confirmed the regulation of gene networks linked to both β-cell function and regeneration. PCA revealed clustering by donor, indicating strong inter-donor variability; this was corrected using ComBat, allowing clearer separation of treatment groups. Differential expression analysis identified 273 DEGs for miR-30d-5p inhibition, 518 for overexpression, and 480 between the two treatments. Key gene changes reflected biological roles aligned with the miRNA’s proposed regulatory function: inhibition of miR-30d-5p upregulated genes linked to stress, immune activation, and metabolism (e.g., GLUT6, TGFB3, CYP4F8), while overexpression enhanced β-cell function and insulin secretion genes (e.g., HOOK1, ISL1, TTR, CACNB3). GO analysis showed that miR-30d-5p inhibition enriched pathways related to protein stress and impaired differentiation, whereas overexpression activated processes involved in ion homeostasis, morphogenesis, and β-cell maintenance. Transcription factor analysis highlighted FOXO3, NOTCH3, JUND, and NR1H2 as potential regulators. Overall, miR-30d-5p promotes β-cell survival, insulin synthesis, and immunoregulation.</description><dates><publication>2026/05/21</publication></dates><accession>GSE316801</accession><cross_references><GSM>GSM9460393</GSM><GSM>GSM9460392</GSM><GSM>GSM9460391</GSM><GSM>GSM9460390</GSM><GSM>GSM9460389</GSM><GSM>GSM9460388</GSM><GSM>GSM9460387</GSM><GSM>GSM9460398</GSM><GSM>GSM9460397</GSM><GSM>GSM9460396</GSM><GSM>GSM9460395</GSM><GSM>GSM9460394</GSM><GPL>24676</GPL><GSE>316801</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>