ArticleVirchows Archiv : an international journal of pathology2005
Transient myofibroblast differentiation of interstitial fibroblastic cells relevant to tubular dilatation in uranyl acetate-induced acute renal failure in rats.
Article in Virchows Archiv : an international journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 52 citations in OpenAlex.
- Despite Its High Salt Content,Food science & nutrition · 2026Article
- In vivo expression of VCAM1 precedes nephron loss following kidney tubular necrosis.Science advances · 2025Article
- Mechanisms of Acute Kidney Injury-Chronic Kidney Disease Transition: Unraveling Maladaptive Repair and Therapeutic Opportunities.Biomolecules · 2025Review
- Defining the molecular fingerprint of bladder and kidney fibroblasts.American journal of physiology. Renal physiology · 2023Review
- Role of perivascular cells in kidney homeostasis, inflammation, repair and fibrosis.Nature reviews. Nephrology · 2023Review
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- The Role of Connexin 43 in Renal Disease: Insights from In Vivo Models of Experimental Nephropathy.International journal of molecular sciences · 2022Review
- Synthetic Retinoids Beyond Cancer Therapy.Annual review of pharmacology and toxicology · 2022Review
- Epigenetic memory contributing to the pathogenesis of AKI-to-CKD transition.Frontiers in molecular biosciences · 2022Review
- Metabolic dysfunction and inflammatory disease: the role of stromal fibroblasts.The FEBS journal · 2021Review
- Fibroblast heterogeneity and tertiary lymphoid tissues in the kidney.Immunological reviews · 2021Review
- Hyperosmotic stress induces epithelial-mesenchymal transition through rearrangements of focal adhesions in tubular epithelial cells.PloS one · 2021Article
- Review
- Fibroblast mTOR/PPARγ/HGF axis protects against tubular cell death and acute kidney injury.Cell death and differentiation · 2019Article
- Early activation of fibroblasts is required for kidney repair and regeneration after injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Progression of chronic kidney disease: too much cellular talk causes damage.Kidney international · 2017Review
- Signaling Crosstalk between Tubular Epithelial Cells and Interstitial Fibroblasts after Kidney Injury.Kidney diseases (Basel, Switzerland) · 2016Review
- Severity and Frequency of Proximal Tubule Injury Determines Renal Prognosis.Journal of the American Society of Nephrology : JASN · 2016Article
- Persistent activation of autophagy in kidney tubular cells promotes renal interstitial fibrosis during unilateral ureteral obstruction.Autophagy · 2016Article
- Wnt/β-catenin signaling in kidney injury and repair: a double-edged sword.Laboratory investigation; a journal of technical methods and pathology · 2016Review
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To investigate the mechanisms of myofibroblast differentiation of interstitial fibroblastic cells (FCs) in rats with uranyl acetate-induced acute renal failure (ARF), we examined the relationship between the expression of alpha-smooth muscle actin (alpha-SMA), myofibroblast phenotype and tubular dilatation as well as cell shape and adhesion of FCs. Peritubular alpha-SMA-positive myofibroblasts appeared after induction of ARF and extended along the damaged, dilated proximal tubules and then almost disappeared after proximal tubular recovery. The perimeter of proximal tubules correlated with fractional areas stained for alpha-SMA (P<0.001). Most alpha-SMA-positive cells did not incorporate [3H]-thymidine, indicating a low proliferative activity. Transmission electron microscopy showed that FCs increasingly attached to the tubular basement membrane by elongated cytoplasm-containing microfilament bundles, which formed abundant adherens and gap junctions from day 4 to day 7. Scanning electron microscopy showed hypertrophic FCs covering large areas of tubules after induction of ARF. Administration of chlorpromazine, which can inhibit cytoskeletal movement, after induction of ARF partially inhibited myofibroblast differentiation of FCs immunohistochemically and morphologically and resulted in more dilated proximal tubules in concert with aggravation of renal dysfunction and inhibition of regenerative repair at day 4 than vehicle-administered rats. Our results indicate that mechanical tension, judged by tubular dilatation, may contribute to the induction of alpha-SMA phenotype with increased stress fiber formation and intercellular junctions in FCs to support damaged nephron structures by adjusting tensional homeostasis in rats with uranyl acetate-induced ARF.
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