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Hemin Impairs Interferon Signaling in Periodontal Cells

ABSTRACT: Hemin has been shown to exert potent immunomodulatory effects in the oral microenvironment, yet its global transcriptional targets remain elusive. In this study, we performed high-throughput Bulk RNA-sequencing to investigate the transcriptomic reprogramming induced by Hemin in human oral epithelial cells (HSC-2) under inflammatory conditions. Our transcriptomic analysis revealed that Hemin effectively reversed the inflammatory signature induced by IL-1β and TNF-α. Specifically, Hemin treatment profoundly and selectively paralyzed the interferon (IFN)-stimulated gene axis (e.g., CXCL10, CXCL11), alongside triggering compensatory NRF2-driven redox stress defenses (e.g., HMOX1). These RNA-seq data provide a comprehensive landscape demonstrating Hemin's role as a targeted repressor that fundamentally uncouples JAK-STAT interferon responses.

ORGANISM(S): Homo sapiens

PROVIDER: GSE335283 | GEO | 2026/06/17

REPOSITORIES: GEO

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	GSE335283_raw_counts_All_Samples.tsv.gz	Tabular

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Project description:We examined, through an oligonucleotide microarray protocol, the renal differential transcriptome profiles of mices submitted to IRI, IPC and Hemin treatment. After identifying the profiles of differentially expressed genes observed for each comparison, we carried out functional enrichment analysis to reveal transcripts putatively involved in potential relevant biological processes and signaling pathways. The most relevant enriched biological processes found in these comparisons were stress, inflammation, apoptosis, pathways in cancer, differentiation, angiogenesis, focal adhesion, ECM-receptor interaction, ion transport, angiogenesis, mitosis and cell cycle, inflammatory response, olfactory transduction and regulation of actin cytoskeleton. In addition, the most important overrepresented pathways were MAPK, ErbB, JAK/STAT, Toll and Nod like receptors, Angiotensin II, Arachidonic acid metabolism, Wnt and coagulation cascade. Also, new insights were gained about the underlying protection mechanisms against renal IRI promoted by IPC and Hemin treatment. Venn diagram analysis allowed us to uncover common and exclusively differentially expressed genes between these two protective maneuvers, underscoring potential common and exclusive biological functions regulated in each case. In summary, IPC exclusively regulated the expression of genes belonging to stress, protein modification and apoptosis, highlighting the role of IPC in controlling exacerbated stress response. Treatment with the Hmox1 inducer Hemin, in turn, exclusively regulated the expression of genes associated with cell differentiation, metabolic pathways, cell cycle, mitosis, development, regulation of actin cytoskeleton and arachidonic acid metabolism, suggesting a pleiotropic effect for Hemin. According to surgery and treatment procedures, mices were divided into five groups: Control, Ischemia-reperfusion injury (IRI), animals pre-treated with Hemin followed by IRI (Hemin + IRI), animals only treated with Hemin (Hemin) and animals pre-conditioned and submitted to IRI (IPC+IRI). To identify the consequences of IRI, Hemin treatment or IPC in gene expression profiles, the following statistical comparisons were made between the groups: IRI vs Control, IPC+IRI vs Control, IPC+IRI vs IRI, IRI+Hemin vs IRI and Hemin vs Control.

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Hemin Impairs Interferon Signaling in Periodontal Cells

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