Evidence map›Paper›PMID 24008336›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2013

MCP-1-induced protein promotes endothelial-like and angiogenic properties in human bone marrow monocytic cells.

Jianli Niu, Kangkai Wang, Olga Zhelyabovska, Yasser Saad, Pappachan E Kolattukudy

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

24 citing papers in PubMed, 33 citations in OpenAlex.

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  11. Activity of MCPIP1 RNase in tumor associated processes.Journal of experimental & clinical cancer research : CR · 2019
    Review
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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 2 institutions in 2 countries.

Jianli NiuBurnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, Florida (J N., O.Z., Y.S., P.E.K.); Department of Pathophysiology, Xiangya School of Medicine, Central South University, Changsha, Hunan, People's Republic of China (K.W.).
Kangkai Wang
Olga Zhelyabovska
Yasser Saad
Pappachan E Kolattukudy
Central South University · CNUniversity of Central Florida · US

Funding

MCP-1 induced gene expression in cardiovascular diseaseR01HL069458 · NHLBI · UNIVERSITY OF CENTRAL FLORIDA · PI KOLATTUKUDY, PAPPACHAN · 2002 to 2005
$1.4M
MCPIP, a novel transcription factor in the development of heart failureR56HL069458 · NHLBI · UNIVERSITY OF CENTRAL FLORIDA · PI KOLATTUKUDY, PAPPACHAN KOLATTUKUDY · 2009 to 2009
$355k
NHLBI NIH HHS HL69458NHLBI NIH HHS R01 HL069458NHLBI NIH HHS R56 HL069458
6 · The paper itself

Abstract

Monocytic cells enhance neovascularization by releasing proangiogenic mediators and/or by transdifferentiating into endothelial-like cells. However, the mechanisms that govern this transdifferentiation process are largely unknown. Recently, monocyte chemotactic protein-1 (MCP-1)-induced protein (MCPIP) has been identified as a novel CCCH-type zinc-finger protein expressed primarily in monocytic cells. Here, we analyzed whether MCPIP might exert angiogenic effects by promoting differentiation of monocytic cells into endothelial cell (EC)-like phenotype. The expression of MCPIP increased during MCP-1-induced transdifferentiation in human bone marrow mononuclear cells (BMNCs). Knockdown of MCPIP with small interfering RNA (siRNA) abolished MCP-1-induced expression of EC markers Flk-1 and Tie-2 in human BMNCs. BMNCs transfected with MCPIP expression vector displayed EC-like morphology accompanied by downregulation of monocytic markers CD14 and CD11b, upregulation of EC markers Flk-1 and Tie-2, induction of cadherin (cdh)-12 and -19, activation of endoplasmic reticulum (ER) stress, and autophagy. Knockdown of cdh-12 or cdh-19 markedly inhibited MCPIP-induced enhancement of cell attachment and EC-marker expression. Inhibition of ER stress by tauroursodeoxycholate abolished MCPIP-induced expression of EC markers. Inhibition of autophagy by knockdown of Beclin-1 with siRNA or by an autophagy inhibitor 3'-methyladenine inhibited MCPIP-induced expression of EC markers. Expression of MCPIP in BMNCs enhanced uptake of acetylated low-density lipoprotein (acLDL), formation of EC-colony, incorporation of cells into capillary-like structure on Matrigel, and exhibited increased neovascularization in the ischemic hindlimb in mice. These results demonstrate that MCPIP may be an important regulator of inflammatory angiogenesis and provide novel mechanistic insights into the link between MCP-1 and cardiovascular diseases.

Indexed as

Neovascularization, PhysiologicAnimalsBlotting, WesternCell Culture TechniquesCell LineCell TransdifferentiationCell TransplantationCollagenCytokinesDrug CombinationsEndothelial CellsEndothelium, VascularHindlimbHumansIschemiaLamininCollagenCytokinesDrug CombinationsLamininmatrigelProteoglycansRibonucleasesRNA, Small InterferingTranscription FactorsZC3H12A protein, human

Identifiers

PMID24008336
PMCPMC3807059
OpenAlexW2055743368

What OpenQuestion holds

Textmetadata
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.