ArticleThe Journal of clinical investigation2018
Polycystin-1 interacts with TAZ to stimulate osteoblastogenesis and inhibit adipogenesis.
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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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.
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.
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Who cites it
48 citing papers in PubMed, 70 citations in OpenAlex.
- Article
- The Important Role of Polycystin in the Skeletal System.Calcified tissue international · 2026Review
- Polycystin-1 and Cardiac Remodeling: From Mechanotransduction to Clinical Consequences.Circulation research · 2026Review
- Autosomal dominant polycystic kidney disease is not a risk factor for scoliosis.International urology and nephrology · 2026Article
- Physiologic mechanisms underlying polycystic kidney disease.Physiological reviews · 2025Review
- Mechanical effects in aging of the musculoskeletal system: Molecular signaling and spatial scale alterations.Journal of orthopaedic translation · 2025Review
- Role of YAP/TAZ in bone diseases: A transductor from mechanics to biology.Journal of orthopaedic translation · 2025Review
- Polycystin-1 regulates tendon-derived mesenchymal stem cells fate and matrix organization in heterotopic ossification.Bone research · 2025Article
- Advanced Piezoelectric Materials, Devices, and Systems for Orthopedic Medicine.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Progress on the mechanism of Polycystin-1 in bone remodeling.Frontiers in cell and developmental biology · 2025Review
- Mechanical protein polycystin-1 directly regulates osteoclastogenesis and bone resorption.Science bulletin · 2024Article
- Runx2 and Polycystins in Bone Mechanotransduction: Challenges for Therapeutic Opportunities.International journal of molecular sciences · 2024Review
- IFT20 and WWTR1 govern bone homeostasis via synchronously regulating the expression and stability of TβRII in osteoblast lineage cells.Research square · 2024Article
- Mechanosensitive protein polycystin-1 promotes periosteal stem/progenitor cells osteochondral differentiation in fracture healing.Theranostics · 2024Article
- Fatty infiltration in the musculoskeletal system: pathological mechanisms and clinical implications.Frontiers in endocrinology · 2024Review
- Article
- Genetic interactions between polycystin-1 and Wwtr1 in osteoblasts define a novel mechanosensing mechanism regulating bone formation in mice.Bone research · 2023Article
- Convergence of Calcium Channel Regulation and Mechanotransduction in Skeletal Regenerative Biomaterial Design.Advanced healthcare materials · 2023Review
- Bone marrow mesenchymal stem cells derived exosomal miRNAs can modulate diabetic bone-fat imbalance.Frontiers in endocrinology · 2023Article
- Woven bone formation and mineralization by rat mesenchymal stromal cells imply increased expression of the intermediate filament desmin.Frontiers in endocrinology · 2023Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
The molecular mechanisms that transduce the osteoblast response to physical forces in the bone microenvironment are poorly understood. Here, we used genetic and pharmacological experiments to determine whether the polycystins PC1 and PC2 (encoded by Pkd1 and Pkd2) and the transcriptional coactivator TAZ form a mechanosensing complex in osteoblasts. Compound-heterozygous mice lacking 1 copy of Pkd1 and Taz exhibited additive decrements in bone mass, impaired osteoblast-mediated bone formation, and enhanced bone marrow fat accumulation. Bone marrow stromal cells and osteoblasts derived from these mice showed impaired osteoblastogenesis and enhanced adipogenesis. Increased extracellular matrix stiffness and application of mechanical stretch to multipotent mesenchymal cells stimulated the nuclear translocation of the PC1 C-terminal tail/TAZ (PC1-CTT/TAZ) complex, leading to increased runt-related transcription factor 2-mediated (Runx2-mediated) osteogenic and decreased PPARγ-dependent adipogenic gene expression. Using structure-based virtual screening, we identified a compound predicted to bind to PC2 in the PC1:PC2 C-terminal tail region with helix:helix interaction. This molecule stimulated polycystin- and TAZ-dependent osteoblastogenesis and inhibited adipogenesis. Thus, we show that polycystins and TAZ integrate at the molecular level to reciprocally regulate osteoblast and adipocyte differentiation, indicating that the polycystins/TAZ complex may be a potential therapeutic target to increase bone mass.
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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.