Challenges in mimicking hypoxia: insights into HIF-regulated MiRNA expression induced by DMOG and CoCl2
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The cellular and tissue response to acute hypoxia is mediated by a complex adaptive response initiated by hypoxia-inducible factors (HIF) 1 and 2. HIF proteins are key transcription factors that modulate gene expression to adapt cells to the low oxygen tension. Cellular studies of hypoxia have used the low oxygen model by using hypoxia chambers to monitor the gene expression changes, while others have utilized hypoxia mimetics in normoxic conditions. Here, we provide a comparison of the utility and limitations of two hypoxia mimetics by studying the changes in the miRNA and mRNA expression profiles compared to the low oxygen model. We utilized data from NGS-based global analyses, qPCR validation, and HIFa silencing experiments to determine the distinct profiles of HIF-1 and HIF-2 activities of the hypoxia and mimetic models. The ability of CoCl 2 and DMOG (dimethyloxalylglycine) to mimic hypoxia was tested in cultured human endothelial cells. The results demonstrated that their treatments resulted in a differential stabilization of HIF-1α and HIF-2α, with CoCl 2 predominantly stabilizing HIF-1α, and DMOG stabilizing HIF-2α. While CoCl 2 and DMOG show potential in mimicking certain isoform-specific effects, their inability to completely mimic their effects on miRNAs and their mRNA targets reveals that these changes do not fully reproduce the hypoxia-induced effects in pathways related to angiogenesis and apoptosis. Taken together, while the hypoxia mimetics offer valuable insights into the isoform-specific effects of HIF-1 and HIF-2, their inability to fully replicate the complexity of hypoxia-induced miRNA interactions is not illustrated in human endothelial cells.
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Pharmacological activation of HIF pathways is predominantly achieved using hypoxia mimetics that inhibit oxygen-dependent HIF degradation.
“Pharmacological activation of HIF pathways is predominantly achieved using hypoxia mimetics [33] that inhibit oxygen-dependent HIF degradation”
From HIF inhibition: Current strategies and clinical challenges (2026) · cites this paper as [33]
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- Authors
- Barton, A., Jaśkiewicz, M., Więch -Walów, A., Moszyńska, A., Cabaj, A., Wielockx, B., Schaefer, L., Collawn, J. F., & Bartoszewski, R.
- Affiliations
- University of Wrocław (PL)
- Gdańsk Medical University (PL)
- Instytut Biologii Doświadczalnej im. Marcelego Nenckiego (PL)
- Technische Universität Dresden (DE)
- Goethe University Frankfurt (DE)
- University of Alabama at Birmingham (US)
- ORCID
- Venue
- Cell Communication and Signaling
- Published
- 2025-10-22
- Volume
- 23
- Issue
- 1
- Pages
- 454-454
- ISSN
- 1478-811X (ISSN-L)
- PMC
- PMC12542114
- OpenAlex
- W4415421867
- Cited by
- 14
- References
- 53
- Citations by year
- 2026: 14
- FWCI
- 6.31
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Cell Communication and Signaling (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- German Research Council (SFB 1177, 259130777 (F11), SFB 1039 (B02), Cardiopulmonary Institute (CPI) (EXC 2026, 390649896), and LOEWE initiative ACLF-I (P08))
- Narodowe Centrum Nauki (UMO-2015/18/E/NZ3/00687)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Health Sciences › Medicine › Hematology › Erythropoietin and Anemia Treatment
- Keywords
- hypoxia mimetics, hypoxia-inducible factor, HIF-1α, HIF-2α, microRNA expression, dimethyloxalylglycine, cobalt chloride, HIF-1α stabilization, human endothelial cells, mRNA expression profiling, angiogenesis, apoptosis, hypoxia
- MeSH terms
- Endothelial PAS Domain-Containing Protein 1, Amino Acids, Dicarboxylic, Cobalt, Gene Expression Regulation, Humans, Cell Hypoxia, MicroRNAs, Basic Helix-Loop-Helix Transcription Factors, Basic Helix-Loop-Helix Proteins, Hypoxia-Inducible Factor 1, alpha Subunit, Human Umbilical Vein Endothelial Cells
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