ArticlePflugers Archiv : European journal of physiology2006
Inconsistent effects of acidosis on HIF-alpha protein and its target genes.
Article in Pflugers Archiv : European journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 47 citations in OpenAlex.
- Gene Expression in Muscle-Invasive and Non-Muscle-Invasive Bladder Cancer Cells Exposed to Hypoxia.Cancers · 2025Article
- Acidosis attenuates the hypoxic stabilization of HIF-1α by activating lysosomal degradation.The Journal of cell biology · 2025Article
- Cell-Type Dependent Regulation of the Electrogenic NaInternational journal of molecular sciences · 2022Article
- The effects of icariin on the expression of HIF-1α, HSP-60 and HSP-70 in PC12 cells suffered from oxygen-glucose deprivation-induced injury.Pharmaceutical biology · 2017Article
- Tumor microenvironment conditions alter Akt and NaBMC cancer · 2017Article
- The progress of angiogenic factors in the development of leukemias.Intractable & rare diseases research · 2016Review
- SDF1 induction by acidosis from principal cells regulates intercalated cell subtype distribution.The Journal of clinical investigation · 2015Article
- Carbonic anhydrase IX, a hypoxia-induced catalytic component of the pH regulating machinery in tumors.Frontiers in physiology · 2014Review
- Preischemic targeting of HIF prolyl hydroxylation inhibits fibrosis associated with acute kidney injury.American journal of physiology. Renal physiology · 2012Article
- Functional interaction between responses to lactic acidosis and hypoxia regulates genomic transcriptional outputs.Cancer research · 2012Article
- Tumor cell metabolism: an integral view.Cancer biology & therapy · 2011Review
- Tumour hypoxia induces a metabolic shift causing acidosis: a common feature in cancer.Journal of cellular and molecular medicine · 2010Review
- Assessment of tumour hypoxia for prediction of response to therapy and cancer prognosis.Journal of cellular and molecular medicine · 2010Review
- A dialogue between the hypoxia-inducible factor and the tumor microenvironment.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2008Article
- Hypoxia and the HIF system in kidney disease.Journal of molecular medicine (Berlin, Germany) · 2007Review
- Three autocrine feedback loops determine HIF1 alpha expression in chronic hypoxia.Biochimica et biophysica acta · 2007Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor HIF-1alpha has been identified as a key regulator in the cellular and systemic response to hypoxia. Because hypoxia is frequently associated with acidosis, like in ischemia or tumour growth, we studied the impact of acidosis on the expression of the HIF-1alpha and HIF-2alpha proteins and that of the three HIF target genes carbonic anhydrase-9 (CA-9), glucose transporter-1 (Glut-1) and erythropoietin (EPO). Since the HIF-prolyl hydroxylases (PHD) modulate cellular HIF-alpha protein levels we also investigated changes in PHD mRNA expression under hypoxia and acidosis. HIF-1alpha immunoblots revealed, depending on the cell line investigated, a moderate induction of HIF-alpha protein levels by acidosis in normoxia (Hep3B cells) or hypoxia (HeLa cells). Concordantly, the activity of HIF-driven luciferase reporters was slightly enhanced at pH 7.0. In contrast, HIF target genes exhibited divergent responses to acidosis: basal and hypoxia-induced CA-9 mRNA levels were further increased, whereas hypoxic EPO mRNA induction was attenuated, and Glut-1 mRNA levels were not altered by acidosis. Except from a small increase of hypoxia-induced PHD3 mRNA levels in HeLa cells, there was also no significant effect of acidosis on PHD expression. In conclusion, albeit HIF protein levels slightly induced by acidosis and the inconsistent regulation of HIF target genes under acidosis suggest additional, yet unidentified pH-sensitive factors to be involved in the regulation of these genes.
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