Evidence map›Paper›PMID 21252071›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2011

Cleaved high-molecular-weight kininogen accelerates the onset of endothelial progenitor cell senescence by induction of reactive oxygen species.

Jihong Dai, Xuemei Zhu, Mervin C Yoder, Yi Wu, Robert W Colman

Open access · greenAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
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  6. Review
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  8. Article
  9. The disulfide isomerase ERp57 is required for fibrin deposition in vivo.Journal of thrombosis and haemostasis : JTH · 2014
    Article
  10. Kallikrein-kinin in stem cell therapy.World journal of stem cells · 2014
    Review
  11. Domain 2 of uPAR regulates single-chain urokinase-mediated angiogenesis through β1-integrin and VEGFR2.American journal of physiology. Heart and circulatory physiology · 2013
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Effects of aging on angiogenesis.Circulation research · 2012
    Review
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

5 authors at 1 institution in 1 country.

Jihong DaiCyrus Tang Hematology Center, Jiangsu Institute of Hematology, First Affiliated Hospital, Soochow University, Suzhou, China.
Xuemei Zhu
Mervin C Yoder
Yi Wu
Robert W Colman
Temple University · US

Funding

Innate Immunity in Experimental Arthritis of KininogenR01AR051713 · NIAMS · TEMPLE UNIV OF THE COMMONWEALTH · PI COLMAN, ROBERT W · 2004 to 2007
$1.2M
The kallikrein-kinin system in endothelial progenitor cell homing in arthritisR03AR057542 · NIAMS · TEMPLE UNIV OF THE COMMONWEALTH · PI WU, YI · 2009 to 2011
$221k
NIAMS NIH HHS AR051713NIAMS NIH HHS AR057542NIAMS NIH HHS R01 AR051713NIAMS NIH HHS R03 AR057542
6 · The paper itself

Abstract

objectiveCleaved high-molecular-weight kininogen (HKa), an activation product of the plasma kallikrein-kinin system, inhibits endothelial cell functions. We questioned whether HKa affects the function of endothelial progenitor cells (EPCs) and accelerates their senescence. METHODS AND

resultsTreatment with HKa for 2 weeks markedly inhibited the formation of large colonies and proliferation of EPCs on collagen surfaces, whereas HKa did not affect collagen-mediated EPC adhesion and survival. Concomitantly, treated EPCs displayed flattened and giant cell morphological changes and formation of intracellular vacuoles. As determined by acidic β-galactosidase staining, HKa increased senescent EPCs by 2- and >3-fold after culture for 1 and 2 weeks, respectively. In addition, HKa suppressed the telomerase activity of EPCs. HKa concentration-dependently increased the generation of intracellular reactive oxygen species (ROS) and markedly upregulated p38 kinase phosphorylation and prosenescence molecule p16(INK4a) expression. SB203580, a p38 inhibitor, attenuated the level of HKa-enhanced p16(INK4a) expression. Either quenching of ROS or inhibition of p38 kinase prevented HKa-induced EPC senescence.

conclusionsHKa accelerates the onset of EPC senescence by activating the ROS-p38 kinase-p16(INK4a) signaling cascade. This novel activity of HKa points out the likelihood of HKa serving as an endogenous inducer of EPC senescence.

Indexed as

Cell ProliferationCellular SenescenceCell AdhesionCells, CulturedCell SurvivalCollagenCyclin-Dependent Kinase Inhibitor p16Endothelial CellsFree Radical ScavengersGreen Fluorescent ProteinsHumansKininogen, High-Molecular-Weightp38 Mitogen-Activated Protein KinasesPhosphorylationProtein Kinase InhibitorsReactive Oxygen SpeciesCollagenCyclin-Dependent Kinase Inhibitor p16enhanced green fluorescent proteinFree Radical ScavengersGreen Fluorescent ProteinsKininogen, High-Molecular-Weightp38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsReactive Oxygen SpeciesTelomerase

Identifiers

PMID21252071
PMCPMC3089907
OpenAlexW2158858343

What OpenQuestion holds

Textmetadata
LicenceTDM
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.