Search bioRxiv⌕ Search

Biology subjects

Ariyeloye, S.

Publications and source records attributed to Ariyeloye, S..

3 recordsLinked to original sources

HIF-1α coordinates adrenal steroidogenesis through direct transcriptional control and regulation of miRNA biogenesis

BackgroundAdrenal steroid hormone production is essential for systemic stress adaptation and metabolic homeostasis, and it is tightly regulated by oxygen availability. Previously, we demonstrated that acute hypoxia suppresses adrenal steroidogenesis through HIF-1-dependent induction of microRNAs (miRNAs) that target key steroidogenic enzymes. However, the mechanisms by which HIF-1 controls miRNA expression and activity in this context remain unclear. MethodsTo address this issue, we mapped the genome-wide HIF-1 binding landscape in murine adrenocortical cells using Cleavage Under Targets & Tagmentation (CUT&Tag). We integrated this data with gene expression analyses following pharmacological HIF-1 stabilization, physiological hypoxia, and genetic HIF-1 depletion to distinguish HIF-1-dependent effects from broader hypoxia-driven responses. ResultsWe detected HIF-1 binding at loci encoding steroidogenic enzymes and steroidogenesis-associated miRNAs. Unexpectedly, we also detected binding at genes involved in miRNA biogenesis and function, including components of the nuclear microprocessor complex and the cytoplasmic RNA-induced silencing complex (RISC). Functional analyses revealed that hypoxia broadly represses the expression of miRNA-processing genes through both HIF-1-dependent and -independent mechanisms. Notably, HIF-1 selectively modulated or counteracted this repression in a gene-specific manner, indicating a regulatory role beyond direct transcriptional activation. ConclusionsThese findings reveal an unrecognized layer of hypoxia-driven cell communication, wherein HIF-1 coordinates the transcriptional and post-transcriptional regulation of adrenal steroidogenesis by shaping the miRNA-processing landscape. This work extends our understanding of how oxygen-sensitive signaling pathways integrate gene expression and RNA-based regulatory mechanisms to control endocrine function.

molecular biology↗

Microbiota-specific serum IgG links gut and joints through immune-endothelial crosstalk in arthritis

Rheumatoid arthritis (RA) pathogenesis involves early gut immune alterations that precede clinical onset and systemic bone involvement. Using mouse and human imaging mass cytometry (IMC) and tissue sequencing, this study shows that intestinal endothelial and immune changes emerge before or coincide with arthritis symptom development. In the collagen-induced arthritis (CIA) model, intestinal vascular permeability and endothelial gene activation promoting leukocyte trafficking appeared prior to synovial inflammation. Spatial mapping of murine and human ileal tissues predicted enhanced epithelial-immune interactions and lymphoid activation, suggesting mucosal immune priming before joint pathology. Both gut-selective 4{beta}7 integrin blockade with vedolizumab and endothelial barrier enhancement by imatinib significantly reduced arthritis severity in CIA mice. After clinical onset, microbiota-specific IgG responses expanded to recognize rare gut bacteria, reflecting increased microbial exposure. Bone marrow endothelium exhibited interferon-I-driven inflammation and vascular activation, indicating tissue-specific endothelial dysfunction. Microbiota-reactive IgG increased during CIA - likely a response to translocating gut bacteria and immune cell activation. Integrating mouse and human data, these findings define a mechanistic framework where endothelial barrier impairment, microbial translocation, and systemic endothelial activation initiate RA autoimmunity, revealing endothelial and mucosal pathways as targets for early intervention. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=145 SRC="FIGDIR/small/702529v1_ufig1.gif" ALT="Figure 1"> View larger version (47K): org.highwire.dtl.DTLVardef@1ef2f41org.highwire.dtl.DTLVardef@77d66org.highwire.dtl.DTLVardef@1b9e4cborg.highwire.dtl.DTLVardef@15bd170_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

HIF1α controls steroidogenesis under acute hypoxic stress

BackgroundHypoxia is a critical physiological and pathological condition known to influence various cellular processes, including steroidogenesis. While previous studies, including our own, have highlighted the regulatory effects of Hypoxia-Inducible Factor 1 (HIF1) on steroid production, the specific molecular mechanisms remain poorly understood. This study investigates the role of hypoxia and HIF1 in steroid biosynthesis across multiple experimental models during acute exposure to low oxygen levels. MethodsTo assess the extent to which acute hypoxia modulates steroidogenesis, we employed several approaches, including the Y1 adrenocortical cell line, an ex vivo adrenal gland explant model, and a conditional HIF1-deficient mouse line in the adrenal cortex. We focused on various regulatory patterns that may critically suppress steroidogenesis. ResultsIn Y1 cells and adrenal gland explants, hypoxia induced the upregulation of specific microRNAs, leading to the suppression of mRNA levels of key steroidogenic enzymes and reduced steroid hormone production. The hypoxia/HIF1-dependent induction of these microRNAs and the consequent modulation of steroid production were confirmed in vivo. Notably, using our conditional HIF1-deficient mouse line, we found that the increase in miRNA expression under hypoxic conditions is directly dependent on HIF1. Furthermore, the regulation of steroidogenic enzymes (e.g., StAR and Cyp11a1) and steroid production occurred at the level of protein translation, revealing an unexpected layer of control under hypoxic conditions in vivo. ConclusionsThese findings elucidate the molecular mechanisms underlying acute hypoxia-induced changes in steroid biosynthesis and may also be useful in developing new strategies for various steroid hormone pathologies.

molecular biology↗