Fig. 1

HIF1α and IRE1α interact during myeloid cell response to hypoxia. A Schematic representation of the OIR mouse model. B Heat map of gene set variation analysis (GSVA) enrichment scores of RNA-seq data from OIR and normoxic retinas at P14 and C P17. Pathways associated with hypoxia response are enriched at P14 when the retina is still avascular, and pathways involved in hypoxia, inflammatory responses and angiogenesis are significantly upregulated at P17 when there is maximal preretinal neovascularization; n = 2–3 mice per condition. For P14, P < 0.05 and > 0.2 logFC and for P17, p adj < 0.05 and > 0.2 logFC. D Immunoblot showing HIF1α stabilization in mononuclear phagocytes (CD45^low, Gr1⁻, CD11b⁺, F4/80⁺) cell-sorted from normoxic and OIR retinas at P14. E STRING database representation of the protein interaction network of HIF1α immunoprecipitated from J774 macrophages under hypoxia (2% O₂ for 8 h) and subjected to tandem mass spectrometry (MS/MS). Proteins including the unfolded protein response (UPR) such as GRP78 are highlighted in blue, and the interaction score ranked from 0 to 1 is noted below. F Co-immunoprecipitation of HIF1α in J774 macrophages under normoxia (21% O₂) and hypoxia (2% O₂) for 1 h followed by immunoblotting (IB) for UPR sensors IRE1α, PERK and ATF6 (n = 3 independent experiments)