ArticleMolecular medicine (Cambridge, Mass.)2022
OLMALINC/OCT4/BMP2 axis enhances osteogenic-like phenotype of renal interstitial fibroblasts to participate in Randall's plaque formation.
Article in Molecular medicine (Cambridge, Mass.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 9 citations in OpenAlex.
- Novel insights into the role of the renal interstitial microenvironment in Randall's plaque formation (Review).International journal of molecular medicine · 2026Review
- FASLG Derived from Fibroblasts in Hydroxyapatite-Rich Microenvironment Induces Urothelial Anoikis to Trigger Randall's Plaque Exposure.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Urolithin A: A Novel Postbiotic for inflammation, aging, and cancer: A Journey from Dietary ellagitannins to clinical use.Molecular biology reports · 2026Review
- Unravelling new mechanisms of occurrence and recurrence in calcium nephrolithiasis: the role of epigenetics.World journal of urology · 2026Review
- Elucidating the pharmacological mechanism of Yangming-Kaixin-Yizhi formula in inhibiting neuronal ferroptosis via Nrf2 in Alzheimer's disease: a study combining network pharmacology, transcriptomics, and experimental validation.Metabolic brain disease · 2026Article
- Establishment and characterization of preclinical model of primary ovarian squamous cell carcinoma.Human cell · 2025Article
- LncRNA OLMALINC promotes osteosarcoma progression through USP1-mediated autophagy suppression.Human cell · 2025Article
- Osteogenic-Like Microenvironment of Renal Interstitium Induced by Osteomodulin Contributes to Randall's Plaque Formation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- A high-calcium environment induced ectopic calcification of renal interstitial fibroblasts via TFPI-2-DCHS1-ALP/ENPP1 axis to participate in Randall's plaque formation.Urolithiasis · 2024Article
- Therapeutic effects of tetrandrine in inflammatory diseases: a comprehensive review.Inflammopharmacology · 2024Review
- Non-Coding RNAs in Kidney Stones.Biomolecules · 2024Review
- Expression of osteogenic proteins in kidneys of cats with nephrocalcinosis.Journal of veterinary internal medicineArticle
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Authors and funding
12 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRandall's plaques (RP) are identified as anchored sites for kidney calcium oxalate stones, but the mechanism remains unclear. Given the importance of osteogenic-like cells in RP formation and OCT4 in reprogramming differentiated cells to osteoblasts, the current study explored the potential role of OCT4 in RP formation.
methodsOCT4 and biomineralization were evaluated in RP, and immunofluorescence co-staining was performed to identify these cells with alteration of OCT4 and osteogenic markers. Based on the analysis of tissue, we further investigated the mechanism of OCT4 in regulating osteogenic-like differentiation of primary human renal interstitial fibroblasts (hRIFs) in vitro and vivo.
resultsWe identified the upregulated OCT4 in RP, with a positive correlation to osteogenic markers. Interestingly, fibroblast marker Vimentin was partially co-localized with upregulated OCT4 and osteogenic markers in RP. Further investigations revealed that OCT4 significantly enhanced the osteogenic-like phenotype of hRIFs in vitro and in vivo. Mechanically, OCT4 directly bound to BMP2 promoter and facilitated its CpG island demethylation to transcriptionally promote BMP2 expression. Furthermore, combination of RIP and RNA profiling uncovered that lncRNA OLMALINC physically interacted with OCT4 to promote its stabilization via disrupting the ubiquitination. Additionally, OLMALINC was upregulated in fibroblasts in RP visualized by FISH, and a positive correlation was revealed between OLMALINC and OCT4 in RP.
conclusionsThe upregulation of OCT4 in hRIFs was a pathological feature of RP formation, and OLMALINC/OCT4/BMP2 axis facilitated hRIFs to acquire osteogenic-like phenotype under osteogenic conditions, through which the pathway might participate in RP formation. Our findings opened up a new avenue to better understand RP formation in which osteogenic-like process was partially triggered by lncRNAs and pluripotency maintenance related genes.
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