Evidence map›Paper›PMID 20601126›Full record

ArticleVascular pharmacology

Molecular mechanism of angiotensin II-induced insulin resistance in aortic vascular smooth muscle cells: roles of Protein Tyrosine Phosphatase-1B.

Pimonrat Ketsawatsomkron, David W Stepp, David J Fulton, Mario B Marrero

Abstract read
In one paragraph

Article in Vascular pharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Angiotensin II Inhibits Insulin Receptor Signaling in Adipose Cells.International journal of molecular sciences · 2022
    Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
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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

4 authors at 1 institution in 1 country.

Pimonrat KetsawatsomkronVascular Biology Center, Medical College of Georgia, Augusta, GA 30912, USA. pim-kets@uiowa.edu
David W Stepp
David J Fulton
Mario B Marrero
Augusta University · US

Funding

Metabolic Determinants of Cardiovascular Dysfunction in ObesityR01HL092446 · NHLBI · AUGUSTA UNIVERSITY · PI FULTON, DAVID J, STEPP, DAVID W · 2009 to 2013
$2.1M
Tyrosine phosphorylation of endothelial nitric oxide synthaseR01HL085827 · NHLBI · AUGUSTA UNIVERSITY · PI FULTON, DAVID J · 2007 to 2011
$1.8M
STRUCTURE AND FUNCTIONS OF UREA TRANSPORTERSP01DK050268 · NIDDK · EMORY UNIVERSITY · PI GUNN, ROBERT B · 1997 to 2002
$1.7M
The Angiotensin II-Induced JAK/STAT Pathway in Diabetes.R01HL058139 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI MARRERO, MARIO BENEDICTO · 1999 to 2005
$1.3M
ANGIOTENSIN II &JAK-STAT PATHWAY IN VASCULAR GROWTHR29HL058139 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI MARRERO, MARIO B. · 1997 to 1998
–
NHLBI NIH HHS HL58139NHLBI NIH HHS R01 HL058139NHLBI NIH HHS R01 HL085827NHLBI NIH HHS R01 HL092446NIDDK NIH HHS DK50268
6 · The paper itself

Abstract

Insulin resistance is an underlying mechanism of type 2 diabetes and its vascular complications. Recent evidence suggests that crosstalk between angiotensin II (Ang II) and the insulin signaling in vascular smooth muscle cell (VSMC) may contribute to cellular insulin resistance. We hypothesized that Ang II inhibits the anti-mitogenic pathways while enhancing the mitogenic pathways stimulated by insulin via activation of Protein Tyrosine Phosphatase-1B (PTP-1B) in VSMC. We found that Ang II significantly inhibited insulin-induced phosphorylation of tyrosine 608 of IRS-1 and serine 473 of Akt, a downstream member of anti-mitogenic pathway of insulin. In contrast, Ang II increased the serine phosphorylation of IRS-1 which was not affected by the presence of insulin. Activation of p42/p44 MAPK (a mitogenic pathway) induced by insulin was further enhanced by Ang II. Transfection of VSMC with PTP-1B antisense oligonucleotide markedly reduced the effects of Ang II on insulin signaling. Furthermore, an increase in VSMC growth was attenuated by PTP-1B antisense only in the presence of both Ang II and insulin. Finally, we also showed that Ang II-induced activation of PTP-1B in VSMC was PKA/JAK2 dependent. We conclude that Ang II modulates both anti-mitogenic and mitogenic pathways of insulin via the activation of PTP-1B.

Indexed as

Angiotensin IIAnimalsAortaCells, CulturedEnzyme ActivationInsulinInsulin ResistanceMaleMyocytes, Smooth MusclePhosphorylationProtein Tyrosine Phosphatase, Non-Receptor Type 1RatsRats, Sprague-DawleySignal TransductionAngiotensin IIInsulinProtein Tyrosine Phosphatase, Non-Receptor Type 1

Identifiers

PMID20601126
PMCPMC4446984
OpenAlexW2021378561

What OpenQuestion holds

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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 OpenQuestion graph.