ArticleMolecular biology of the cell2014
The fate of the primary cilium during myofibroblast transition.
Article in Molecular biology of the cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed.
- Primary cilium disassembly - from mechanisms to roles in physiology and disease.Journal of cell science · 2026Review
- The primary cilium at the helm: gatekeeper of TGF-β superfamily signaling in development, homeostasis, and disease.Biochemical Society transactions · 2026Review
- Centrosomal JAK2 Tyrosine Kinase Regulates Primary Cilia Length, Cell Proliferation, and Cilia Orientation During Cell Migration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Imbalance of Ciliary Programs Drives Fibroblast Differentiation and Fibrotic Signaling in Systemic Sclerosis.bioRxiv : the preprint server for biology · 2026Article
- Broadening horizons: new links between cilia and heart development and disease.Frontiers in cardiovascular medicine · 2026Review
- Endocardial primary cilia and blood flow regulate EndoMT during endocardial cushion development.Nature cardiovascular research · 2025Article
- Cilia at the crossroad: convergence of regulatory mechanisms to govern cilia dynamics during cell signaling and the cell cycle.Cell & bioscience · 2025Review
- CYLD/HDAC6 signaling regulates the interplay between epithelial-mesenchymal transition and ciliary homeostasis during pulmonary fibrosis.Cell death & disease · 2024Article
- The implication of ciliary signaling pathways for epithelial-mesenchymal transition.Molecular and cellular biochemistry · 2024Review
- Primary cilia suppress the fibrotic activity of atrial fibroblasts from patients with atrial fibrillation in vitro.Scientific reports · 2024Article
- Transport and barrier mechanisms that regulate ciliary compartmentalization and ciliopathies.Nature reviews. Nephrology · 2024Review
- Cep120 is essential for kidney stromal progenitor cell growth and differentiation.EMBO reports · 2024Article
- Primary cilia and actin regulatory pathways in renal ciliopathies.Frontiers in nephrology · 2023Review
- Article
- Review
- An EMT-primary cilium-GLIS2 signaling axis regulates mammogenesis and claudin-low breast tumorigenesis.Science advances · 2021Article
- Myocardin-related transcription factor and serum response factor regulate cilium turnover by both transcriptional and local mechanisms.iScience · 2021Article
- MRTF: Basic Biology and Role in Kidney Disease.International journal of molecular sciences · 2021Review
- Genetic Background and Clinicopathologic Features of Adult-onset Nephronophthisis.Kidney international reports · 2021Article
- Mutations in the Kinesin-2 Motor KIF3B Cause an Autosomal-Dominant Ciliopathy.American journal of human genetics · 2020Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Myofibroblasts, the culprit of organ fibrosis, can originate from mesenchymal and epithelial precursors through fibroblast-myofibroblast and epithelial-myofibroblast transition (EMyT). Because certain ciliopathies are associated with fibrogenesis, we sought to explore the fate and potential role of the primary cilium during myofibroblast formation. Here we show that myofibroblast transition from either precursor results in the loss of the primary cilium. During EMyT, initial cilium growth is followed by complete deciliation. Both EMyT and cilium loss require two-hit conditions: disassembly/absence of intercellular contacts and transforming growth factor-β1 (TGFβ) exposure. Loss of E-cadherin-dependent junctions induces cilium elongation, whereas both stimuli are needed for deciliation. Accordingly, in a scratch-wounded epithelium, TGFβ provokes cilium loss exclusively along the wound edge. Increased contractility, a key myofibroblast feature, is necessary and sufficient for deciliation, since constitutively active RhoA, Rac1, or myosin triggers, and down-regulation of myosin or myocardin-related transcription factor prevents, this process. Sustained myosin phosphorylation and consequent deciliation are mediated by a Smad3-, Rac1-, and reactive oxygen species-dependent process. Transitioned myofibroblasts exhibit impaired responsiveness to platelet-derived growth factor-AA and sonic hedgehog, two cilium-associated stimuli. Although the cilium is lost during EMyT, its initial presence contributes to the transition. Thus myofibroblasts represent a unique cilium-less entity with profoundly reprogrammed cilium-related signaling.
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