Evidence map›Paper›PMID 34934133›Full record

ArticleScientific reports2021

MEK inhibition exerts temporal and myeloid cell-specific effects in the pathogenesis of neurofibromatosis type 1 arteriopathy.

Rebekah Tritz, Farlyn Z Hudson, Valerie Harris, Pushpankur Ghoshal, Bhupesh Singla, Huiping Lin, Gabor Csanyi, Brian K Stansfield

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 37% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Article
  3. 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

8 authors at 1 institution in 1 country.

Rebekah TritzVascular Biology Center, Augusta University, Augusta, GA, USA.
Farlyn Z HudsonVascular Biology Center, Augusta University, Augusta, GA, USA.
Valerie HarrisVascular Biology Center, Augusta University, Augusta, GA, USA.
Pushpankur GhoshalVascular Biology Center, Augusta University, Augusta, GA, USA.
Bhupesh SinglaVascular Biology Center, Augusta University, Augusta, GA, USA.
Huiping LinVascular Biology Center, Augusta University, Augusta, GA, USA.
Gabor CsanyiVascular Biology Center, Augusta University, Augusta, GA, USA.
Brian K StansfieldVascular Biology Center, Augusta University, Augusta, GA, USA. bstansfield@augusta.edu.
Augusta University Health · US

Funding

Inflammation and retinopathy of prematurityR01EY029318 · NEI · AUGUSTA UNIVERSITY · PI STANSFIELD, BRIAN KEVIN · 2019 to 2023
$2.2M
Lipid macropinocytosis: a novel target in atherosclerotic cardiovascular diseaseR01HL139562 · NHLBI · AUGUSTA UNIVERSITY · PI CSANYI, GABOR · 2018 to 2022
$1.9M
Regulation of Lymphangiogenesis by Thrombospondin 1R00HL146954 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI SINGLA, BHUPESH · 2022 to 2024
$739k
Regulation of Lymphangiogenesis by Thrombospondin 1K99HL146954 · NHLBI · AUGUSTA UNIVERSITY · PI SINGLA, BHUPESH · 2020 to 2021
$232k
NEI NIH HHS R01 EY029318NHLBI NIH HHS K99 HL146954NHLBI NIH HHS R00 HL146954NHLBI NIH HHS R01 HL139562
6 · The paper itself

Abstract

Mutations in the NF1 tumor suppressor gene are linked to arteriopathy. Nf1 heterozygosity (Nf1+/-) results in robust neointima formation, similar to humans, and myeloid-restricted Nf1+/- recapitulates this phenotype via MEK-ERK activation. Here we define the contribution of myeloid subpopulations to NF1 arteriopathy. Neutrophils from WT and Nf1+/- mice were functionally assessed in the presence of MEK and farnesylation inhibitors in vitro and neutrophil recruitment to lipopolysaccharide was assessed in WT and Nf1+/- mice. Littermate 12-15 week-old male wildtype and Nf1+/- mice were subjected to carotid artery ligation and provided either a neutrophil depleting antibody (1A8), liposomal clodronate to deplete monocytes/macrophages, or PD0325901 and neointima size was assessed 28 days after injury. Bone marrow transplant experiments assessed monocyte/macrophage mobilization during neointima formation. Nf1+/- neutrophils exhibit enhanced proliferation, migration, and adhesion via p21

Indexed as

AnimalsBone Marrow CellsCarotid Artery InjuriesMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutMitogen-Activated Protein Kinase KinasesMonocytesMyeloid Progenitor CellsNeointimaNeurofibromatosis 1Neurofibromin 1Receptors, CCR2Ccr2 protein, mouseMitogen-Activated Protein Kinase KinasesNeurofibromin 1Receptors, CCR2

Identifiers

PMID34934133
PMCPMC8692602
OpenAlexW4200160780

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.