ArticleJournal of biomedical science2025
Regulation of the mechanoresponsive Neat1 and PSPC1 by substrate stiffness in TGF-β1-induced renal progenitor cell fate.
Article in Journal of biomedical science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
backgroundPhysical differences between acute kidney injury and chronic kidney disease, particularly in matrix stiffness, may influence mesenchymal stem cells to promote either regeneration or fibrosis; however, the underlying mechanisms remain unclear. Here, we investigate the role of paraspeckles and the long non-coding RNA Neat1 in TGF-β1-induced stem cell fate determination.
methodsMouse kidney progenitor cells (MKPCs) were cultured on stiff (collagen-coated dishes) and soft (type I collagen gel) matrices and treated with TGF-β1. RNA sequencing and subsequent bioinformatic analyses were performed to identify transcriptional differences between cells on stiff and soft matrices under TGF-β1 stimulation. Western-blotting and qPCR were used to quantify target proteins and RNA levels. Immunofluorescence staining and RNA fluorescence in situ hybridization were conducted to examine the subcellular localization of proteins and RNAs. Loss-of-function and gain-of-function experiments were performed using siRNA, shRNA, pharmacological inhibitors and expression vector.
resultsWe found that TGF-β1 induced MKPC differentiation into myofibroblasts on stiff matrices or endothelial-like cells on soft matrices. Matrix stiffness regulated PSPC1 and Neat1 to trigger either TGF-β1-induced transdifferentiation into myofibroblasts or angiogenesis on soft collagen gels. Stiff matrices increased the expression levels of Neat1 and PSPC1, whereas soft matrices reduced their expressions. Knockdown of PSPC1 impaired myofibroblast differentiation on stiff matrices and partially reduced angiogenesis on soft matrices. On stiff matrices, TGF-β1 markedly reduced Neat1 levels, potentially releasing PSPC1 to interact with pSmad2/3 and activate EMT-related gene expression, thereby promoting myofibroblast activation. Furthermore, we identified two mechanosensory pathways that PSPC1 and Neat1 responded to mechanical signals via β1-integrin-YAP and Piezo1 pathways.
conclusionsThis study links mechano-regulation of paraspeckle complex to TGF-β1-induced renal mesenchymal stem cell fate, providing insights into mechanotransduction and nuclear signaling in kidney fibrosis and regeneration.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.