ArticlePloS one2014
An upregulation in the expression of vanilloid transient potential channels 2 enhances hypotonicity-induced cytosolic Ca²⁺ rise in human induced pluripotent stem cell model of Hutchinson-Gillford Progeria.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 21 citations in OpenAlex.
- Ameliorating calcium homeostasis improves longevity and healthspan in progeroid and naturally aged mice.Nature communications · 2026Article
- Universal multilayer network embedding reveals a causal link between GABA neurotransmitter and cancer.BMC bioinformatics · 2025Article
- Endothelial cell-specific progerin expression does not cause cardiovascular alterations and premature death.Aging cell · 2025Article
- Cellular reprogramming as a tool to model human aging in a dish.Nature communications · 2024Review
- High-Throughput Screen Detects Calcium Signaling Dysfunction in Hutchinson-Gilford Progeria Syndrome.International journal of molecular sciences · 2021Article
- Endoplasmic reticulum stress at the crossroads of progeria and atherosclerosis.EMBO molecular medicine · 2019Article
- Differential stem cell aging kinetics in Hutchinson-Gilford progeria syndrome and Werner syndrome.Protein & cell · 2018Article
- Induced Pluripotent Stem Cells to Study Mechanisms of Laminopathies: Focus on Epigenetics.Frontiers in cell and developmental biology · 2018Review
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hutchinson-Gillford Progeria Syndrome (HGPS) is a fatal genetic disorder characterized by premature aging in multiple organs including the skin, musculoskeletal and cardiovascular systems. It is believed that an increased mechanosensitivity of HGPS cells is a causative factor for vascular cell death and vascular diseases in HGPS patients. However, the exact mechanism is unknown. Transient receptor potential (TRP) channels are cationic channels that can act as cellular sensors for mechanical stimuli. The aim of this present study was to examine the expression and functional role of TRP channels in human induced pluripotent stem cell-derived endothelial cells (iPSC-ECs) from the patients with HGPS. The mRNA and protein expression of TRP channels in HGPS and control (IMR90) iPSC-ECs were examined by semi-quantitative RT-PCRs and immunoblots, respectively. Hypotonicity-induced cytosolic Ca²⁺ ([Ca²⁺](i)) rise in iPSC-ECs was measured by confocal microscopy. RT-PCRs and immunoblots showed higher expressional levels of TRPV2 in iPSC-ECs from HGPS patients than those from normal individuals. In functional studies, hypotonicity induced a transient [Ca²⁺](i) rise in iPSC-ECs from normal individuals but a sustained [Ca²⁺](i) elevation in iPSC-ECs from HGPS patients. A nonselective TRPV inhibitor, ruthenium red (RuR, 20 µM), and a specific TRPV2 channel inhibitor, tranilast (100 µM), abolished the sustained phase of hypotonicity-induced [Ca²⁺](i) rise in iPSC-ECs from HGPS patients, and also markedly attenuated the transient phase of the [Ca²⁺](i) rise in these cells. Importantly, a short 10 min hypotonicity treatment caused a substantial increase in caspase 8 activity in iPSC-ECs from HGPS patients but not in cells from normal individuals. Tranilast could also inhibit the hypotonicity-induced increase in caspase 8 activity. Taken together, our data suggest that an up-regulation in TRPV2 expression causes a sustained [Ca²⁺](i) elevation in HGPS-iPSC-ECs under hypotonicity, consequently resulting in apoptotic cell death. This mechanism may contribute to the pathogenesis of vascular diseases in HGPS patients.
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