Transcriptomic profiling of miR-383-overexpressing and senescent human dermal fibroblasts

This dataset accompanies the manuscript “miR-383 promotes senescence in human dermal fibroblasts by targeting PCLAF and suppressing DNA repair”. The study tests the hypothesis that miR-383 promotes human dermal fibroblast senescence by suppressing DNA repair-associated transcriptional programs and targeting PCLAF/KIAA0101.

The Excel workbook contains four supplementary tables:
Table S1: Differential expression results comparing human dermal fibroblasts transfected with miR-383 mimic versus control mimic.
Table S2: Gene Ontology Biological Process enrichment results for genes altered upon miR-383 overexpression.
Table S3: Reactome pathway enrichment results for genes altered upon miR-383 overexpression.
Table S4: Differential expression results comparing late-passage senescent human dermal fibroblasts with early-passage proliferating fibroblasts.
The data show that miR-383 overexpression induces broad transcriptional changes in human dermal fibroblasts, with prominent downregulation of genes and pathways associated with cell-cycle progression, DNA replication, DNA repair, and the DNA damage response. Comparison with replicative senescence-associated transcriptomic changes shows that miR-383 overexpression suppresses transcriptional programs that overlap with those repressed during fibroblast senescence.

The microarray data were generated from RNA isolated from cultured human dermal fibroblasts and analyzed to identify differentially expressed genes and enriched biological pathways. Differential expression tables include gene-level statistics such as fold change and significance values, while enrichment tables summarize overrepresented Gene Ontology or Reactome pathways among the affected genes.

These data can be used to examine the transcriptional effects of miR-383 in human dermal fibroblasts, identify miR-383-regulated candidate genes, explore biological pathways associated with fibroblast senescence, and compare miR-383-induced transcriptional changes with those observed during replicative senescence.