Evidence map›Paper›PMID 24947528›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2014

Transplanted perivascular adipose tissue accelerates injury-induced neointimal hyperplasia: role of monocyte chemoattractant protein-1.

David Manka, Tapan K Chatterjee, Lynn L Stoll, Joshua E Basford, Eddy S Konaniah, Ramprasad Srinivasan, Vladimir Y Bogdanov, Yaoliang Tang, Andra L Blomkalns, David Y Hui and 1 more

Open access · greenAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

72 citing papers in PubMed, 118 citations in OpenAlex.

  1. Trial
  2. Review
  3. Adipokine Nesfatin-1 Mediates Endothelial Dysfunction by SuppressingJournal of the American Heart Association · 2026
    Article
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  8. Review
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  10. Article
  11. Pericarotid Fat as a Marker of Cerebrovascular Risk.AJNR. American journal of neuroradiology · 2024
    Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
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  20. Article

12 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

David MankaFrom the Department of Internal Medicine, Division of Cardiovascular Diseases (D.M.), Department of Pathology and Laboratory Medicine (J.E.B., E.S.K., D.Y.H.), Department of Internal Medicine, Division of Hematology/Oncology (R.S., V.Y.B.), and Department of Emergency Medicine (A.L.B.), University of Cincinnati, OH; Department of Internal Medicine, Vascular Biology Center, Georgia Regents University, Augusta (T.K.C., Y.T., N.L.W.); and Department of Emergency Medicine, University of Iowa, Iowa City (retired) (L.L.S.).
Tapan K ChatterjeeFrom the Department of Internal Medicine, Division of Cardiovascular Diseases (D.M.), Department of Pathology and Laboratory Medicine (J.E.B., E.S.K., D.Y.H.), Department of Internal Medicine, Division of Hematology/Oncology (R.S., V.Y.B.), and Department of Emergency Medicine (A.L.B.), University of Cincinnati, OH; Department of Internal Medicine, Vascular Biology Center, Georgia Regents University, Augusta (T.K.C., Y.T., N.L.W.); and Department of Emergency Medicine, University of Iowa, Iowa City (retired) (L.L.S.). tchatterjee@gru.edu.
Lynn L StollFrom the Department of Internal Medicine, Division of Cardiovascular Diseases (D.M.), Department of Pathology and Laboratory Medicine (J.E.B., E.S.K., D.Y.H.), Department of Internal Medicine, Division of Hematology/Oncology (R.S., V.Y.B.), and Department of Emergency Medicine (A.L.B.), University of Cincinnati, OH; Department of Internal Medicine, Vascular Biology Center, Georgia Regents University, Augusta (T.K.C., Y.T., N.L.W.); and Department of Emergency Medicine, University of Iowa, Iowa City (retired) (L.L.S.).
Joshua E BasfordFrom the Department of Internal Medicine, Division of Cardiovascular Diseases (D.M.), Department of Pathology and Laboratory Medicine (J.E.B., E.S.K., D.Y.H.), Department of Internal Medicine, Division of Hematology/Oncology (R.S., V.Y.B.), and Department of Emergency Medicine (A.L.B.), University of Cincinnati, OH; Department of Internal Medicine, Vascular Biology Center, Georgia Regents University, Augusta (T.K.C., Y.T., N.L.W.); and Department of Emergency Medicine, University of Iowa, Iowa City (retired) (L.L.S.).
Eddy S KonaniahFrom the Department of Internal Medicine, Division of Cardiovascular Diseases (D.M.), Department of Pathology and Laboratory Medicine (J.E.B., E.S.K., D.Y.H.), Department of Internal Medicine, Division of Hematology/Oncology (R.S., V.Y.B.), and Department of Emergency Medicine (A.L.B.), University of Cincinnati, OH; Department of Internal Medicine, Vascular Biology Center, Georgia Regents University, Augusta (T.K.C., Y.T., N.L.W.); and Department of Emergency Medicine, University of Iowa, Iowa City (retired) (L.L.S.).
Ramprasad SrinivasanFrom the Department of Internal Medicine, Division of Cardiovascular Diseases (D.M.), Department of Pathology and Laboratory Medicine (J.E.B., E.S.K., D.Y.H.), Department of Internal Medicine, Division of Hematology/Oncology (R.S., V.Y.B.), and Department of Emergency Medicine (A.L.B.), University of Cincinnati, OH; Department of Internal Medicine, Vascular Biology Center, Georgia Regents University, Augusta (T.K.C., Y.T., N.L.W.); and Department of Emergency Medicine, University of Iowa, Iowa City (retired) (L.L.S.).
Vladimir Y BogdanovFrom the Department of Internal Medicine, Division of Cardiovascular Diseases (D.M.), Department of Pathology and Laboratory Medicine (J.E.B., E.S.K., D.Y.H.), Department of Internal Medicine, Division of Hematology/Oncology (R.S., V.Y.B.), and Department of Emergency Medicine (A.L.B.), University of Cincinnati, OH; Department of Internal Medicine, Vascular Biology Center, Georgia Regents University, Augusta (T.K.C., Y.T., N.L.W.); and Department of Emergency Medicine, University of Iowa, Iowa City (retired) (L.L.S.).
Yaoliang TangFrom the Department of Internal Medicine, Division of Cardiovascular Diseases (D.M.), Department of Pathology and Laboratory Medicine (J.E.B., E.S.K., D.Y.H.), Department of Internal Medicine, Division of Hematology/Oncology (R.S., V.Y.B.), and Department of Emergency Medicine (A.L.B.), University of Cincinnati, OH; Department of Internal Medicine, Vascular Biology Center, Georgia Regents University, Augusta (T.K.C., Y.T., N.L.W.); and Department of Emergency Medicine, University of Iowa, Iowa City (retired) (L.L.S.).
Andra L BlomkalnsFrom the Department of Internal Medicine, Division of Cardiovascular Diseases (D.M.), Department of Pathology and Laboratory Medicine (J.E.B., E.S.K., D.Y.H.), Department of Internal Medicine, Division of Hematology/Oncology (R.S., V.Y.B.), and Department of Emergency Medicine (A.L.B.), University of Cincinnati, OH; Department of Internal Medicine, Vascular Biology Center, Georgia Regents University, Augusta (T.K.C., Y.T., N.L.W.); and Department of Emergency Medicine, University of Iowa, Iowa City (retired) (L.L.S.).
David Y HuiFrom the Department of Internal Medicine, Division of Cardiovascular Diseases (D.M.), Department of Pathology and Laboratory Medicine (J.E.B., E.S.K., D.Y.H.), Department of Internal Medicine, Division of Hematology/Oncology (R.S., V.Y.B.), and Department of Emergency Medicine (A.L.B.), University of Cincinnati, OH; Department of Internal Medicine, Vascular Biology Center, Georgia Regents University, Augusta (T.K.C., Y.T., N.L.W.); and Department of Emergency Medicine, University of Iowa, Iowa City (retired) (L.L.S.).
Neal L WeintraubFrom the Department of Internal Medicine, Division of Cardiovascular Diseases (D.M.), Department of Pathology and Laboratory Medicine (J.E.B., E.S.K., D.Y.H.), Department of Internal Medicine, Division of Hematology/Oncology (R.S., V.Y.B.), and Department of Emergency Medicine (A.L.B.), University of Cincinnati, OH; Department of Internal Medicine, Vascular Biology Center, Georgia Regents University, Augusta (T.K.C., Y.T., N.L.W.); and Department of Emergency Medicine, University of Iowa, Iowa City (retired) (L.L.S.).
Georgia Regents Medical Center · USAugusta University · US

Funding

LCenter for Clinical and Translational Science and TrainingUL1TR001425 · NCATS · UNIVERSITY OF CINCINNATI · PI HEUBI, JAMES E., KISSELA, BRETT M · 2015 to 2024
$37.5M
Role of Lipoprotein Receptors in Diet-induced Obesity and DiabetesR01DK074932 · NIDDK · UNIVERSITY OF CINCINNATI · PI HUI, DAVID YIU-KWAN · 2007 to 2019
$4.4M
Hypoxia and cardiac stem cell homingR01HL086555 · NHLBI · UNIVERSITY OF CINCINNATI · PI TANG, YAO LIANG · 2008 to 2019
$3.5M
Angiotensin II, oxidative stress, and aneurysm formationR01HL076684 · NHLBI · UNIVERSITY OF IOWA · PI WEINTRAUB, NEAL L · 2005 to 2013
$3.0M
Perivascular adipose tissue and vascular remodelingR01HL112640 · NHLBI · UNIVERSITY OF CINCINNATI · PI WEINTRAUB, NEAL L · 2012 to 2016
$2.1M
Innate Immunity, CD14 Signaling, and Abdominal Aortic AneurysmsK08HL105675 · NHLBI · UNIVERSITY OF CINCINNATI · PI BLOMKALNS, ANDRA LEAH · 2012 to 2015
$550k
NCATS NIH HHS UL1 TR001425NHLBI NIH HHS HL076684NHLBI NIH HHS HL086555NHLBI NIH HHS HL105675NHLBI NIH HHS HL112640NHLBI NIH HHS K08 HL105675NHLBI NIH HHS R01 HL076684NHLBI NIH HHS R01 HL086555NHLBI NIH HHS R01 HL112640NIDDK NIH HHS DK74932NIDDK NIH HHS R01 DK074932
6 · The paper itself

Abstract

objectivePerivascular adipose tissue (PVAT) expands during obesity, is highly inflamed, and correlates with coronary plaque burden and increased cardiovascular risk. We tested the hypothesis that PVAT contributes to the vascular response to wire injury and investigated the underlying mechanisms. APPROACH AND

resultsWe transplanted thoracic aortic PVAT from donor mice fed a high-fat diet to the carotid arteries of recipient high-fat diet-fed low-density lipoprotein receptor knockout mice. Two weeks after transplantation, wire injury was performed, and animals were euthanized 2 weeks later. Immunohistochemistry was performed to quantify adventitial macrophage infiltration and neovascularization and neointimal lesion composition and size. Transplanted PVAT accelerated neointimal hyperplasia, adventitial macrophage infiltration, and adventitial angiogenesis. The majority of neointimal cells in PVAT-transplanted animals expressed α-smooth muscle actin, consistent with smooth muscle phenotype. Deletion of monocyte chemoattractant protein-1 in PVAT substantially attenuated the effects of fat transplantation on neointimal hyperplasia and adventitial angiogenesis, but not adventitial macrophage infiltration. Conditioned medium from perivascular adipocytes induced potent monocyte chemotaxis in vitro and angiogenic responses in cultured endothelial cells.

conclusionsThese findings indicate that PVAT contributes to the vascular response to wire injury, in part through monocyte chemoattractant protein-1-dependent mechanisms.

Indexed as

NeointimaActinsAdipocytesAdipose TissueAnimalsBiomarkersCarotid ArteriesCarotid Artery InjuriesCells, CulturedChemokine CCL2ChemotaxisCoculture TechniquesCulture Media, ConditionedDiet, High-FatDisease Models, AnimalEndothelial CellsActinsalpha-smooth muscle actin, mouseBiomarkersCcl2 protein, mouseChemokine CCL2Culture Media, ConditionedReceptors, LDLadipose tissuehyperplasia

Identifiers

PMID24947528
PMCPMC4103955
OpenAlexW2529648316

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.