ArticleBiochemical and biophysical research communications2008
Osmotically-induced genes are controlled by the transcription factor TonEBP in cultured cardiomyocytes.
Article in Biochemical and biophysical research communications, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- NFAT5: a stress-related transcription factor with multiple functions in health and disease.Cell stress · 2025Review
- Chronic high‑salt intake induces cardiomyocyte autophagic vacuolization during left ventricular maladaptive remodeling in spontaneously hypertensive rats.Experimental and therapeutic medicine · 2023Article
- Sperm preparedness and adaptation to osmotic and pH stressors relate to functional competence of sperm in Bos taurus.Scientific reports · 2021Article
- NFAT5-Mediated Signalling Pathways in Viral Infection and Cardiovascular Dysfunction.International journal of molecular sciences · 2021Review
- Elevated extracellular glucose and uncontrolled type 1 diabetes enhance NFAT5 signaling and disrupt the transverse tubular network in mouse skeletal muscle.Experimental biology and medicine (Maywood, N.J.) · 2012Article
- The role of hyperosmotic stress in inflammation and disease.Biomolecular concepts · 2012Article
- Macromolecular crowding regulates assembly of mRNA stress granules after osmotic stress: new role for compatible osmolytes.The Journal of biological chemistry · 2012Article
- The transcription factor NFAT5 is required for cyclin expression and cell cycle progression in cells exposed to hypertonic stress.PloS one · 2009Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Changes in cardiac osmolarity occur in myocardial infarction. Osmoregulatory mechanisms may, therefore, play a crucial role in cardiomyocyte survival. Tonicity-responsive enhancer binding protein (TonEBP) is a key transcription factor participating in the adaptation of cells to increases in tonicity. However, it is unknown whether cardiac TonEBP is activated by tonicity. Hypertonicity activated transcriptional activity of TonEBP, increased the amounts of both TonEBP mRNA and protein, and induced both the mRNA and protein of TonEBP target genes (aldose reductase and heat shock protein-70). Hypotonicity decreased the amount of TonEBP protein indicating bidirectional osmoregulation of this transcription factor. Adenoviral expression of a dominant negative TonEBP suppressed the hypertonicity-dependent increase of aldose reductase protein. These results indicated that TonEBP controls osmoregulatory mechanisms in cardiomyocytes.
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