ArticleCell biology international2025
Bufalin-Induced Epithelial-to-Mesenchymal Transition in Kidney Epithelial Cells.
Article in Cell biology international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Bufalin-Induced Epithelial-to-Mesenchymal Transition in Kidney Epithelial Cells.Cell biology international · 2025Article
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4 authors.
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Abstract
The kidney plays a central role in fluid, electrolyte, and blood pressure regulation, processes tightly coupled to Na⁺/K⁺-ATPase activity. Beyond its canonical transport function, Na⁺/K⁺-ATPase also acts as a signaling receptor for cardiotonic steroids (CTSs) such as bufalin, which have been implicated in fibrosis and epithelial-to-mesenchymal transition (EMT). Here, we investigated the effects of serial passages on porcine kidney epithelial LLC-PK1 cells and their response to the endogenous CTS bufalin. High-passage cells (P > 80) displayed increased proliferation (1.7x), viability (1.5x), and migration (2.2x) compared to low-passage cells (P < 40), concomitant with elevated ERK1/2 phosphorylation (2.5x), while NKA activity and expression remained unchanged. Bufalin treatment (20 nM, 48 h) induced striking morphological changes consistent with EMT in P > 80 cells, including a transition from cuboidal to elongated shapes with cytoplasmic extensions, whereas P < 40 cells were largely resistant. In high-passage cells, bufalin reduced pan-cadherin, E-cadherin, occludin, claudin-1, ZO-1, and ZO-2 expression, with redistribution of adhesion proteins from membrane to cytoplasm. β-catenin and ZEB-1 were excluded from the nucleus, indicating altered transcriptional regulation during EMT. In contrast, low-passage cells exhibited only modest reductions in E-cadherin, claudin-1, and ZEB-1, along with increased ZO-2, and β-catenin expression. For comparison, TGF-β1 induced partial EMT features in bufalin-resistant LLC-PK1 cells, including striking cell elongation, increased vimentin expression, and appearance of E-cadherin aggregates. Together, these results demonstrate that bufalin induces EMT-like changes in LLC-PK1 cells in a passage-dependent manner, possibly through ERK1/2 activation, disruption of intercellular adhesion, and modulation of transcription factor localization. These findings highlight bufalin as a regulator of epithelial plasticity with potential implications for renal pathophysiology.
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