Evidence mapPaperPMID 27933336Full record

ArticleDiabetologia2017

SHP-1 activation inhibits vascular smooth muscle cell proliferation and intimal hyperplasia in a rodent model of insulin resistance and diabetes.

Weier Qi, Qian Li, Chong Wee Liew, Christian Rask-Madsen, Samuel M Lockhart, Lars Melholt Rasmussen, Yu Xia, Xuanchun Wang, Mogher Khamaisi, Kevin Croce and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Diabetologia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

15 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  3. Platelet Membrane-Encapsulated Poly(lactic-International journal of pharmaceutics: X · 2024
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  9. Pathogenesis and Clinical Significance of In-Stent Restenosis in Patients with Diabetes.International journal of environmental research and public health · 2021
    Review
  10. Review
  11. Article
  12. Observational
  13. Review
  14. Article
  15. 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

11 authors at 4 institutions in 2 countries.

Weier QiResearch Division, Joslin Diabetes Center, Harvard Medical School, Dianne Nunnally Hoppes Laboratories, One Joslin Place, Boston, MA, 02215, USA.
Qian LiResearch Division, Joslin Diabetes Center, Harvard Medical School, Dianne Nunnally Hoppes Laboratories, One Joslin Place, Boston, MA, 02215, USA.
Chong Wee LiewDepartment of Physiology and Biophysics, University of Illinois at Chicago, Chicago, IL, USA.
Christian Rask-MadsenResearch Division, Joslin Diabetes Center, Harvard Medical School, Dianne Nunnally Hoppes Laboratories, One Joslin Place, Boston, MA, 02215, USA.
Samuel M LockhartResearch Division, Joslin Diabetes Center, Harvard Medical School, Dianne Nunnally Hoppes Laboratories, One Joslin Place, Boston, MA, 02215, USA.
Lars Melholt RasmussenDepartment of Clinical Biochemistry and Pharmacology, Center for Individualized Medicine in Arterial Diseases (CIMA), Odense University Hospital, Odense, Denmark.
Yu XiaResearch Division, Joslin Diabetes Center, Harvard Medical School, Dianne Nunnally Hoppes Laboratories, One Joslin Place, Boston, MA, 02215, USA.
Xuanchun WangResearch Division, Joslin Diabetes Center, Harvard Medical School, Dianne Nunnally Hoppes Laboratories, One Joslin Place, Boston, MA, 02215, USA.
Mogher KhamaisiResearch Division, Joslin Diabetes Center, Harvard Medical School, Dianne Nunnally Hoppes Laboratories, One Joslin Place, Boston, MA, 02215, USA.
Kevin CroceCardiovascular Clinical Research Center, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
George L KingResearch Division, Joslin Diabetes Center, Harvard Medical School, Dianne Nunnally Hoppes Laboratories, One Joslin Place, Boston, MA, 02215, USA. George.King@Joslin.harvard.edu.
Harvard University · USJoslin Diabetes Center · USOdense University Hospital · DKUniversity of Illinois Chicago · US

Funding

PILOT STUDY--SECRETORY TARGETING IN PANCREATIC B CELLSP30DK036836 · JOSLIN DIABETES CENTER · 1986 to 2025
$12.1M
SELECTIVE INSULIN RESISTANCE--DIABETIC VASCULAR DISEASER01DK053105 · JOSLIN DIABETES CENTER · 1997 to 2005
$995k
NIDDK NIH HHS K99 DK090210NIDDK NIH HHS P30 DK036836NIDDK NIH HHS R00 DK090210NIDDK NIH HHS R01 DK053105
6 · The paper itself

Abstract

aims/hypothesisAccelerated migration and proliferation of vascular smooth muscle cells (VSMCs) enhances arterial restenosis after angioplasty in insulin resistance and diabetes. Elevation of Src homology 2-containing protein tyrosine phosphatase 1 (SHP-1) induces apoptosis in the microvasculature. However, the role of SHP-1 in intimal hyperplasia and restenosis has not been clarified in insulin resistance and diabetes.

methodsWe used a femoral artery wire injury mouse model, rodent models with insulin resistance and diabetes, and patients with type 2 diabetes. Further, we modulated SHP-1 expression using a transgenic mouse that overexpresses SHP-1 in VSMCs (Shp-1-Tg). SHP-1 agonists were also employed to study the molecular mechanisms underlying the regulation of SHP-1 by oxidised lipids.

resultsMice fed a high-fat diet (HFD) exhibited increased femoral artery intimal hyperplasia and decreased arterial SHP-1 expression compared with mice fed a regular diet. Arterial SHP-1 expression was also decreased in Zucker fatty rats, Zucker diabetic fatty rats and in patients with type 2 diabetes. In primary cultured VSMCs, oxidised LDL suppressed SHP-1 expression by activating Mek-1 (also known as Map2k1) and increased DNA methylation of the Shp-1 promoter. VSMCs from Shp-1-Tg mice exhibited impaired platelet-derived growth factor (PDGF)-stimulated tyrosine phosphorylation with a concomitant decrease in PDGF-stimulated VSMC proliferation and migration. Similarly, HFD-fed Shp-1-Tg mice and mice treated with the SHP-1 inducer, Icariside II, were protected from the development of intimal hyperplasia following wire injury. CONCLUSIONS/

interpretationSuppression of SHP-1 by oxidised lipids may contribute to the excessive VSMC proliferation, inflammatory cytokine production and intimal hyperplasia observed in arteries from diabetes and insulin resistance. Augmenting SHP-1 levels is a potential therapeutic strategy to maintain stent patency in patients with insulin resistance and diabetes.

Indexed as

AnimalsBlotting, WesternCell CycleCell MovementCell ProliferationHumansHyperplasiaInsulin ResistanceMiceMice, Inbred C57BLMice, TransgenicMuscle, Smooth, VascularMyocytes, Smooth MuscleProtein Tyrosine Phosphatase, Non-Receptor Type 6RatsRats, ZuckerProtein Tyrosine Phosphatase, Non-Receptor Type 6DiabetesInsulin resistanceRestenosisSHP-1

Identifiers

PMID27933336
PMCPMC5672905
OpenAlexW2560631484

What Socratic holds

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LicenceCC BY
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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 Socratic graph.