ArticlePloS one2021
Hyperosmotic stress induces epithelial-mesenchymal transition through rearrangements of focal adhesions in tubular epithelial cells.
Article in PloS one, 2021. 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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16 citing papers in PubMed, 23 citations in OpenAlex.
- An Acidic Tubulointerstitial Microenvironment Delays Cell-Cycle Progression in Proximal Tubule Cells and Fibroblasts and Synergizes With Lactate to Drive Phenotypic Alterations.Acta physiologica (Oxford, England) · 2026Article
- Differential Transcriptomic and Adhesion Responses of Human Periodontal Ligament Cells to Cyclic and Static Hydrostatic Pressure.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Cellular Responses to Mechanical Cues Across Scales: From Fundamental Insights to Translational Potential.Advanced healthcare materials · 2026Review
- Pressure-mediated mechanosensitive Piezo2 channel is activated in neurogenic bladder and promote bladder fibrosis in children.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Deciphering the impact ofGenes & diseases · 2026Article
- BPGM shapes NFAT5-driven cellular responses.Cellular and molecular life sciences : CMLS · 2026Article
- From glucosuria to dialysis: a case report of osmotic nephropathy due to an SGLT2 inhibitor.BMC nephrology · 2026Article
- Article
- Osmotic stress inhibits osteoblast differentiation and mineralization by suppressing TRPV4-mediated calcium influx.Journal of bone and mineral metabolism · 2025Article
- Hyperosmotic Stress Promotes the Nuclear Translocation of TFEB in Tubular Epithelial Cells Depending on Intracellular CaCellular and molecular bioengineering · 2025Article
- Y-27632 targeting ROCK1&2 modulates cell growth, fibrosis and epithelial-mesenchymal transition in hyperplastic prostate by inhibiting β-catenin pathway.Molecular biomedicine · 2024Article
- Modelling and targeting mechanical forces in organ fibrosis.Nature reviews bioengineering · 2024Article
- Hydrostatic pressure mediates epithelial-mesenchymal transition of cholangiocytes through RhoA/ROCK and TGF-β/smad pathways.PloS one · 2024Article
- High Salt Promotes Inflammatory and Fibrotic Response in Peritoneal Cells.International journal of molecular sciences · 2023Article
- Immersion Fixation and Staining of Multicubic Millimeter Volumes for Electron Microscopy-Based Connectomics of Human Brain Biopsies.Biological psychiatry · 2023Article
- Ion channels as a therapeutic target for renal fibrosis.Frontiers in physiology · 2022Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-mesenchymal transition (EMT) of tubular epithelial cells is a hallmark of renal tubulointerstitial fibrosis and is associated with chronic renal injury as well as acute renal injury. As one of the incidences and risk factors for acute renal injury, increasing the osmolality in the proximal tubular fluid by administration of intravenous mannitol has been reported, but the detailed mechanisms remain unclear. Hyperosmotic conditions caused by mannitol in the tubular tissue may generate not only osmotic but also mechanical stresses, which are known to be able to induce EMT in epithelial cells, thereby contributing to renal injury. Herein, we investigate the effect of hyperosmolarity on EMT in tubular epithelial cells. Normal rat kidney (NRK)-52E cells were exposed to mannitol-induced hyperosmotic stress. Consequently, the hyperosmotic stress led to a reduced expression of the epithelial marker E-cadherin and an enhanced expression of the mesenchymal marker, α-smooth muscle actin (α-SMA), which indicates an initiation of EMT in NKR-52E cells. The hyperosmotic condition also induced time-dependent disassembly and rearrangements of focal adhesions (FAs) concomitant with changes in actin cytoskeleton. Moreover, prevention of FAs rearrangements by cotreatment with Y-27632, a Rho-associated protein kinase inhibitor, could abolish the effects of hyperosmotic mannitol treatment, thus attenuating the expression of α-SMA to the level in nontreated cells. These results suggest that hyperosmotic stress may induce EMT through FAs rearrangement in proximal tubular epithelial cells.
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