ArticleHuman molecular genetics2011
Endothelial cells from humans and mice with polycystic kidney disease are characterized by polyploidy and chromosome segregation defects through survivin down-regulation.
Article in Human molecular genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 70 citations in OpenAlex.
- Endothelial dysfunction and oxidative stress in polycystic kidney disease.American journal of physiology. Renal physiology · 2014Trial
- The Mechanosensitive Pkd2 Channel Modulates the Recruitment of Myosin II and Actin to the Cytokinetic Contractile Ring.Journal of fungi (Basel, Switzerland) · 2024Article
- Identifying the roles of miR-17 in ciliogenesis and cell cycle.Frontiers in cell and developmental biology · 2024Article
- Folate conjugated nanomedicines for selective inhibition of mTOR signaling in polycystic kidneys at clinically relevant doses.Biomaterials · 2023Article
- Polycystin-1 Interacting Protein-1 (CU062) Interacts with the Ectodomain of Polycystin-1 (PC1).Cells · 2023Article
- Tubular-specific expression of HIV protein Vpr leads to severe tubulointerstitial damage accompanied by progressive fibrosis and cystic development.Kidney international · 2023Article
- Brain microvascular endothelial cells possess a second cilium that arises from the daughter centriole.Frontiers in molecular biosciences · 2023Article
- Single-cell RNA sequencing reveals differential cell cycle activity in key cell populations during nephrogenesis.Scientific reports · 2021Article
- Epithelial proliferation and cell cycle dysregulation in kidney injury and disease.Kidney international · 2021Review
- Differential modulation of SK channel subtypes by phosphorylation.Cell calcium · 2021Article
- Portal hypertension: An uncommon presentation of Caroli's syndrome.Clinical case reports · 2020Article
- Exploring Key Challenges of Understanding the Pathogenesis of Kidney Disease in Bardet-Biedl Syndrome.Kidney international reports · 2020Review
- Rapamycin treatment correlates changes in primary cilia expression with cell cycle regulation in epithelial cells.Biochemical pharmacology · 2020Article
- Collateral Vessels Have Unique Endothelial and Smooth Muscle Cell Phenotypes.International journal of molecular sciences · 2019Article
- Article
- Caroli syndrome: a clinical case with detailed histopathological analysis.Clinical journal of gastroenterology · 2019Article
- Polycystin and calcium signaling in cell death and survival.Cell calcium · 2018Review
- IFT proteins spatially control the geometry of cleavage furrow ingression and lumen positioning.Nature communications · 2017Article
- RAPAMYCIN INCREASES LENGTH AND MECHANOSENSORY FUNCTION OF PRIMARY CILIA IN RENAL EPITHELIAL AND VASCULAR ENDOTHELIAL CELLS.International education and research journal · 2016Article
- Capillary endothelia from two ADPKD patients are polyploidy.Annals of clinical cytology and pathology · 2016Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Autosomal-dominant polycystic kidney disease (ADPKD) is the most common hereditary and systemic disorder associated with various cardiovascular complications. It has been implicated with dysfunction in primary cilia. We and others have shown that the immediate function of endothelial cilia is to sense extracellular signal. The long-term function of cilia is hypothesized to regulate cell cycle. Here, we show that ciliary function (polycystins) and structure (polaris) are required for proper cellular division. Cilia mutant cells undergo abnormal cell division with apparent defects in mitotic spindle formation, cellular spindle assembly checkpoint and centrosome amplification. Down-regulation of the chromosomal passenger survivin contributes to these abnormalities, which further result in cell polyploidy. Re-expression of survivin restores a competent spindle assembly checkpoint and reduces polyploidy. Aged animals show a more severe phenotype in cellular division, consistent with progression of cardiovascular complications seen in older ADPKD patients. For the first time, we show that structure and function of mechanosensory cilia are crucial in maintaining proper cellular proliferation. Furthermore, developmental aging plays a crucial role in the progression of these abnormal cellular phenotypes. We propose that abnormal function or structure of primary cilia not only causes failure to transmit extracellular signals, but also is associated with cytokinesis defects in both mice and humans with polycystic kidney disease.
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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.