ArticleMediators of inflammation2012
NFAT5 contributes to osmolality-induced MCP-1 expression in mesothelial cells.
Article in Mediators of inflammation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- The Role of NF-κB in Peritoneal Fibrosis and Adhesion in Humans and Animals: A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Unraveling the pleiotropic effects of CCR2-dependent signal transduction in fibrosis development.Theranostics · 2026Review
- Hyperosmolar stress induces monocyte chemoattractant protein 1 expression in retinal pigmented epithelial arising retinal pigmented epithelial 19 cells.Molecular vision · 2025Article
- NFAT5: a stress-related transcription factor with multiple functions in health and disease.Cell stress · 2025Review
- Involvement of CCL2 in Salivary Gland Response to Hyperosmolar Stress Related to Sjögren's Syndrome.International journal of molecular sciences · 2024Article
- High Salt Promotes Inflammatory and Fibrotic Response in Peritoneal Cells.International journal of molecular sciences · 2023Article
- Tissue Sodium Accumulation Induces Organ Inflammation and Injury in Chronic Kidney Disease.International journal of molecular sciences · 2023Review
- Article
- NFAT5-Mediated Signalling Pathways in Viral Infection and Cardiovascular Dysfunction.International journal of molecular sciences · 2021Review
- Potential Role of Gene Regulator NFAT5 in the Pathogenesis of Diabetes Mellitus.Journal of diabetes research · 2020Review
- Autocrine MCP-1/CCR2 signaling stimulates proliferation and migration of renal carcinoma cells.Oncology letters · 2016Article
- Article
- Renal systems biology of patients with systemic inflammatory response syndrome.Kidney international · 2015Observational
- The potential role of NFAT5 and osmolarity in peritoneal injury.BioMed research international · 2015Review
- Extracellular osmolarity regulates matrix homeostasis in the intervertebral disc and articular cartilage: evolving role of TonEBP.Matrix biology : journal of the International Society for Matrix Biology · 2014Review
- Focal adhesion kinase regulates the activity of the osmosensitive transcription factor TonEBP/NFAT5 under hypertonic conditions.Frontiers in physiology · 2014Article
- Generation of a conditional knockout allele for the NFAT5 gene in mice.Frontiers in physiology · 2014Article
- NFAT5 in cellular adaptation to hypertonic stress - regulations and functional significance.Journal of molecular signaling · 2013Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increased expression of the C-C chemokine monocyte chemoattractant protein-1 (MCP-1) in mesothelial cells in response to high glucose concentrations and/or high osmolality plays a crucial role in the development of peritoneal fibrosis during continuous ambulatory peritoneal dialysis (CAPD). Recent studies suggest that in kidney cells osmolality-induced MCP-1 upregulation is mediated by the osmosensitive transcription factor, nuclear factor of activated T cells 5 (NFAT5). The present study addressed the question of whether activation of NFAT5 by hyperosmolality, as present in PD fluids, contributes to MCP-1 expression in the mesothelial cell line Met5A. Hyperosmolality, induced by addition of glucose, NaCl, or mannitol to the growth medium, increased NFAT5 activity and stimulated MCP-1 expression in Met5A cells. siRNA-mediated knockdown of NFAT5 attenuated osmolality-induced MCP-1 upregulation substantially. Hyperosmolality also induced activation of nuclear factor-κB (NF-κB). Accordingly, pharmacological inhibition of NF-κB significantly decreased osmolality-induced MCP-1 expression. Taken together, these results indicate that high osmolalities activate the transcription factor NFAT5 in mesothelial cells. NFAT5 in turn upregulates MCP-1, likely in combination with NF-κB, and thus may participate in the development of peritoneal fibrosis during CAPD.
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