Evidence map›Paper›PMID 24463424›Full record

ArticleThe Journal of investigative dermatology2014

Elevated circulation levels of an antiangiogenic SERPIN in patients with diabetic microvascular complications impair wound healing through suppression of Wnt signaling.

Jeffrey D McBride, Alicia J Jenkins, Xiaochen Liu, Bin Zhang, Kyungwon Lee, William L Berry, Ralf Janknecht, Courtney T Griffin, Christopher E Aston, Timothy J Lyons and 2 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of investigative dermatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 75 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
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  6. Targeting Signalling Pathways in Chronic Wound Healing.International journal of molecular sciences · 2023
    Review
  7. Article
  8. Article
  9. Article
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  15. Article
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  17. Diabetes-induced upregulation of kallistatin levels exacerbates diabetic nephropathy via RAS activation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  18. Review
  19. Review
  20. Article
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 2 institutions in 2 countries.

Jeffrey D McBrideDepartment of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA; Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA; Harold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
Alicia J JenkinsHarold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA; NHMRC Clinical Trials Centre, University of Sydney, Sydney, New South Wales, Australia.
Xiaochen LiuDepartment of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA; Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA; Harold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
Bin ZhangDepartment of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
Kyungwon LeeDepartment of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA; Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA; Harold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
William L BerryDepartment of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
Ralf JanknechtDepartment of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
Courtney T GriffinDepartment of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA; Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA.
Christopher E AstonDepartment of Pediatrics, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
Timothy J LyonsHarold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
James J TomasekDepartment of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA.
Jian-Xing MaDepartment of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA; Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA; Harold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA. Electronic address: jian-xing-ma@ouhsc.edu.
University of Oklahoma Health Sciences Center · USUniversity of Sydney · AU

Funding

THE ROLE OF COMPLEX 1 IN MITOCHONDRIAL DYSFUNCTION & FREE RADICAL PROD IN TYPE 1P20RR024215 · NCRR · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI SHORT, KEVIN R. · 2007 to 2011
$11.7M
Project 5 VEGF Signaling in PhotoreceptorsP20GM104934 · NIGMS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI LE, YUN ZHENG · 2012 to 2016
$10.8M
A new pathogenic mechanism for diabetic retinopathyR01EY019309 · NEI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Jian-Xing Jay Ma · 2009 to 2026
$6.1M
The wnt signaling pathway in choroidal neovascularizationR01EY018659 · NEI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI MA, JIAN-XING · 2009 to 2019
$3.7M
NCRR NIH HHS P20 RR024215NEI NIH HHS R01 EY018659NEI NIH HHS R01 EY019309NIGMS NIH HHS P20 GM104934
6 · The paper itself

Abstract

Wound healing, angiogenesis, and hair follicle maintenance are often impaired in the skin of diabetic patients, but the pathogenesis has not been well understood. Here, we report that circulation levels of kallistatin, a member of the serine proteinase inhibitor (SERPIN) superfamily with antiangiogenic activities, were elevated in type 2 diabetic patients with diabetic vascular complications. To test the hypothesis that elevated kallistatin levels could contribute to a wound-healing deficiency via the inhibition of Wnt/β-catenin signaling, we generated kallistatin-transgenic (KS-TG) mice. KS-TG mice had reduced cutaneous hair-follicle density, microvascular density, and panniculus adiposus layer thickness, as well as altered skin microvascular hemodynamics and delayed cutaneous wound healing. Using Wnt reporter mice, our results showed that Wnt/β-catenin signaling is suppressed in the dermal endothelium and hair follicles in KS-TG mice. Lithium, a known activator of β-catenin via inhibition of glycogen synthase kinase-3β, reversed the inhibition of Wnt/β-catenin signaling by kallistatin and rescued the wound-healing deficiency in KS-TG mice. These observations suggest that elevated circulating antiangiogenic serpins in diabetic patients may contribute to impaired wound healing through inhibition of Wnt/β-catenin signaling. Activation of Wnt/β-catenin signaling, at a level downstream of Wnt receptors, may ameliorate the wound-healing deficiency in diabetic patients.

Indexed as

Gene Expression RegulationWnt Signaling PathwayWound HealingAdultAnimalsCells, CulturedDiabetes Mellitus, Type 2Diabetic AngiopathiesFemaleGenes, ReporterGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHair FollicleHumansLithiumMaleGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanGsk3b protein, mousekallistatinLithiumSerpins

Identifiers

PMID24463424
PMCPMC4065799
OpenAlexW2080122517

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.