Evidence map›Paper›PMID 31680061›Full record

ArticleStem cell reports2019

Closing the Mitochondrial Permeability Transition Pore in hiPSC-Derived Endothelial Cells Induces Glycocalyx Formation and Functional Maturation.

Gesa L Tiemeier, Gangqi Wang, Sébastien J Dumas, Wendy M P J Sol, M Cristina Avramut, Tobias Karakach, Valeria V Orlova, Cathelijne W van den Berg, Christine L Mummery, Peter Carmeliet and 2 more

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
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  7. Article
  8. Mitochondrial Permeability Transition in Stem Cells, Development, and Disease.Advances in experimental medicine and biology · 2023
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 2 countries.

Gesa L TiemeierThe Einthoven Laboratory for Vascular and Regenerative Medicine, Department of Internal Medicine, Division of Nephrology, Leiden University Medical Center, Leiden, The Netherlands.
Gangqi WangThe Einthoven Laboratory for Vascular and Regenerative Medicine, Department of Internal Medicine, Division of Nephrology, Leiden University Medical Center, Leiden, The Netherlands.
Sébastien J DumasLaboratory of Angiogenesis and Vascular Metabolism, Department of Oncology, KU Leuven, Leuven, Belgium; Laboratory of Angiogenesis and Vascular Metabolism, Center for Cancer Biology, VIB, Leuven, Belgium.
Wendy M P J SolThe Einthoven Laboratory for Vascular and Regenerative Medicine, Department of Internal Medicine, Division of Nephrology, Leiden University Medical Center, Leiden, The Netherlands.
M Cristina AvramutDepartment of Cell and Chemical Biology, Section Electron Microscopy, Leiden University Medical Center, Leiden, The Netherlands.
Tobias KarakachLaboratory of Angiogenesis and Vascular Metabolism, Department of Oncology, KU Leuven, Leuven, Belgium; Laboratory of Angiogenesis and Vascular Metabolism, Center for Cancer Biology, VIB, Leuven, Belgium.
Valeria V OrlovaDepartment of Anatomy and Embryology, Leiden University Medical Center, Leiden, The Netherlands.
Cathelijne W van den BergThe Einthoven Laboratory for Vascular and Regenerative Medicine, Department of Internal Medicine, Division of Nephrology, Leiden University Medical Center, Leiden, The Netherlands.
Christine L MummeryDepartment of Anatomy and Embryology, Leiden University Medical Center, Leiden, The Netherlands.
Peter CarmelietLaboratory of Angiogenesis and Vascular Metabolism, Department of Oncology, KU Leuven, Leuven, Belgium; Laboratory of Angiogenesis and Vascular Metabolism, Center for Cancer Biology, VIB, Leuven, Belgium.
Bernard M van den BergThe Einthoven Laboratory for Vascular and Regenerative Medicine, Department of Internal Medicine, Division of Nephrology, Leiden University Medical Center, Leiden, The Netherlands.
Ton J RabelinkThe Einthoven Laboratory for Vascular and Regenerative Medicine, Department of Internal Medicine, Division of Nephrology, Leiden University Medical Center, Leiden, The Netherlands. Electronic address: a.j.rabelink@lumc.nl.
Leiden University Medical Center · NLKU Leuven · BEVIB-KU Leuven Center for Cancer Biology · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human induced pluripotent stem cells (hiPSCs) are used to study organogenesis and model disease as well as being developed for regenerative medicine. Endothelial cells are among the many cell types differentiated from hiPSCs, but their maturation and stabilization fall short of that in adult endothelium. We examined whether shear stress alone or in combination with pericyte co-culture would induce flow alignment and maturation of hiPSC-derived endothelial cells (hiPSC-ECs) but found no effects comparable with those in primary microvascular ECs. In addition, hiPSC-ECs lacked a luminal glycocalyx, critical for vasculature homeostasis, shear stress sensing, and signaling. We noted, however, that hiPSC-ECs have dysfunctional mitochondrial permeability transition pores, resulting in reduced mitochondrial function and increased reactive oxygen species. Closure of these pores by cyclosporine A improved EC mitochondrial function but also restored the glycocalyx such that alignment to flow took place. These results indicated that mitochondrial maturation is required for proper hiPSC-EC functionality.

Indexed as

Cell DifferentiationCell LineEndothelial CellsGlycocalyxHumansInduced Pluripotent Stem CellsMitochondriaMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreReactive Oxygen SpeciesMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreReactive Oxygen Speciescyclosporine Aendothelial cell differentiationglycocalyxhiPSC-derived endothelial cellshiPSC-ECsmaturationmitochondrial dysfunctionmitochondrial permeability transition porereactive oxygen speciesshear stress

Identifiers

PMID31680061
PMCPMC6895683
OpenAlexW2987688255

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.