ArticleScientific reports2019
Polycystin-1 Regulates Actomyosin Contraction and the Cellular Response to Extracellular Stiffness.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- An integrin beta-1-anchored bicaudal C1-polycystin-1 module essential for tubular morphogenesis in polycystic kidney disease.iScience · 2026Article
- Cilia-to-basement membrane signaling is a biomechanical driver in models of autosomal dominant polycystic kidney disease.The Journal of clinical investigation · 2026Article
- The exocyst in ciliogenesis.Renal failure · 2025Review
- Extra-ciliary role for polycystins in regulation of Ezrin and renal tubular morphology.bioRxiv : the preprint server for biology · 2025Article
- Polycystin-1 Mutant Alters Mechanotransduction in Response to Collagen and Extracellular Matrix Stiffness via Daam1-Dependent Microfilament Remodeling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Genome editing strategies to generate working models of polycystic kidney disease.Scientific reports · 2025Article
- Prostaglandin Analogs and Eupatilin as Treatments for Nephronophthisis.Kidney international reports · 2025Article
- Physiologic mechanisms underlying polycystic kidney disease.Physiological reviews · 2025Review
- Review
- Decoupling shear stress and pressure effects in the biomechanics of autosomal dominant polycystic kidney disease using a perfused kidney-on-chip.bioRxiv : the preprint server for biology · 2024Article
- Computational study of biomechanical drivers of renal cystogenesis.Biomechanics and modeling in mechanobiology · 2023Article
- Vascular mechanotransduction.Physiological reviews · 2023Review
- Review of the Use of Animal Models of Human Polycystic Kidney Disease for the Evaluation of Experimental Therapeutic Modalities.Journal of clinical medicine · 2023Review
- Article
- Tracking N- and C-termini of C. elegans polycystin-1 reveals their distinct targeting requirements and functions in cilia and extracellular vesicles.PLoS genetics · 2022Article
- Polycystin-1 and hydrostatic pressure are implicated in glioblastoma pathogenesis in vitro.Journal of cellular and molecular medicine · 2022Article
- The GPCR properties of polycystin-1- A new paradigm.Frontiers in molecular biosciences · 2022Review
- Urinary exosome proteomic profiling defines stage-specific rapid progression of autosomal dominant polycystic kidney disease and tolvaptan efficacy.BBA advances · 2021Article
- A Multitubular Kidney-on-Chip to Decipher Pathophysiological Mechanisms in Renal Cystic Diseases.Frontiers in bioengineering and biotechnology · 2021Article
- Insights Into the Molecular Mechanisms of Polycystic Kidney Diseases.Frontiers in physiology · 2021Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polycystin-1 (PC-1) and 2 (PC-2) are the products of the PKD1 and PKD2 genes, which are mutated in Autosomal Dominant Polycystic Kidney Disease (ADPKD). They form a receptor/channel complex that has been suggested to function as a mechanosensor, possibly activated by ciliary bending in the renal tubule, and resulting in calcium influx. This model has recently been challenged, leaving the question as to which mechanical stimuli activate the polycystins still open. Here, we used a SILAC/Mass-Spec approach to identify intracellular binding partners of tagged-endogenous PC-1 whereby we detected a class of interactors mediating regulation of cellular actomyosin contraction. Accordingly, using gain and loss-of-function cellular systems we found that PC-1 negatively regulates cellular contraction and YAP activation in response to extracellular stiffness. Thus, PC-1 enables cells to sense the rigidity of the extracellular milieu and to respond appropriately. Of note, in an orthologous murine model of PKD we found evidence of increased actomyosin contraction, leading to enhanced YAP nuclear translocation and transcriptional activity. Finally, we show that inhibition of ROCK-dependent actomyosin contraction by Fasudil reversed YAP activation and significantly improved disease progression, in line with recent studies. Our data suggest a possible direct role of PC-1 as a mechanosensor of extracellular stiffness.
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