Evidence map›Paper›PMID 21420414›Full record

ArticleJournal of molecular and cellular cardiology2011

Vascular smooth muscle Jak2 deletion prevents angiotensin II-mediated neointima formation following injury in mice.

Annet Kirabo, S Paul Oh, Hideko Kasahara, Kay-Uwe Wagner, Peter P Sayeski

Abstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

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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

5 authors at 3 institutions in 1 country.

Annet KiraboDepartment of Physiology and Functional Genomics, University of Florida College of Medicine, Gainesville, FL 32610, USA.
S Paul Oh
Hideko Kasahara
Kay-Uwe Wagner
Peter P Sayeski
Florida College · USUniversity of Florida · USUniversity of Nebraska Medical Center · US

Funding

The Role of Jak2 in Angiotensin II SignalingR01HL067277 · NHLBI · UNIVERSITY OF FLORIDA · PI SAYESKI, PETER P · 2002 to 2011
$2.9M
NHLBI NIH HHS R01 HL067277NHLBI NIH HHS R01-HL67277
6 · The paper itself

Abstract

The in vitro treatment of vascular smooth muscle cells (VSMC) with angiotensin II (Ang II) causes Janus kinase 2 (Jak2) to interact with the Ang II type 1 receptor (AT(1)-R) resulting in enhanced cell growth. However, the role that Jak2 plays in AT(1)-R-mediated vascular cell growth and remodeling in vivo is less clear. We hypothesized that in vivo, Jak2 plays a rate-limiting role in Ang II-mediated neointima formation following vascular injury. Using the Cre-loxP system, we conditionally ablated Jak2 from the VSMC of mice. We found that these mice are protected from Ang II-mediated neointima formation following iron chloride-induced vascular injury. In addition, the VSMC Jak2 null mice were protected from injury-induced vascular fibrosis and the pathological loss of the contractile marker, smooth muscle α-actin. Finally, when compared to controls, the VSMC Jak2 null mice exhibited significantly less Ang II-induced VSMC proliferation and migration in vitro and in vivo and more apoptosis. These results suggest that Jak2 plays a central role in the causation of Ang II-induced neointima formation following vascular injury and may provide a novel target for the prevention of neointima formation.

Indexed as

NeointimaActinsAngiotensin IIAnimalsApoptosisCell MovementCell ProliferationCell SurvivalDisease Models, AnimalFemaleFibrosisJanus Kinase 2MaleMiceMice, KnockoutMuscle, Smooth, VascularActinsAngiotensin IIJanus Kinase 2STAT3 Transcription FactorSTAT5 Transcription Factor

Identifiers

PMID21420414
PMCPMC3092026
OpenAlexW2125389970

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.