Evidence map›Paper›PMID 25409512›Full record

ArticlePloS one2014

Differential regulation of human aortic smooth muscle cell proliferation by monocyte-derived macrophages from diabetic patients.

Te-Chuan Chen, Mao-Ling Sung, Hsing-Chun Kuo, Shao-Ju Chien, Chia-Kuang Yen, Cheng-Nan Chen

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Omics research in atherosclerosis.Molecular and cellular biochemistry · 2025
    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

6 authors at 4 institutions in 1 country.

Te-Chuan ChenDivision of Nephrology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Mao-Ling SungDepartment of Cardiology, St. Martin De Porres Hospital, Chiayi, Taiwan.
Hsing-Chun KuoInstitute of Nursing and Department of Nursing, Chang Gung University of Science and Technology, Chronic Diseases and Health Promotion Research Center, CGUST, Taoyuan, Taiwan; Research Center for Industry of Human Ecology, Chang Gung University of Science and Technology, Taoyuan, Taiwan.
Shao-Ju ChienDivision of Pediatric Cardiology, Department of Pediatrics, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Chia-Kuang YenDepartment of Cardiology, St. Martin De Porres Hospital, Chiayi, Taiwan.
Cheng-Nan ChenDepartment of Biochemical Science and Technology, National Chiayi University, Chiayi, Taiwan.
Kaohsiung Chang Gung Memorial Hospital · TWSt. Martin de Porres Hospital · TWChang Gung University of Science and Technology · TWNational Chiayi University · TW

Funding

NTP INFORMATION SYSTEMS SUPPORT27305C0011 · NIEHS · Z-TECH CORPORATION · 2007 to 2009
$4.3M
PROVIDE RABBITS, RATS, MICE, HAMSTERS, GERBILS, GUINEA PIGS27307C0011 · NIEHS · PI BOLEN, WAYNE · 2007 to 2007
$500k
NIEHS NIH HHS 27305C0011NIEHS NIH HHS 27307C0011NIEHS NIH HHS 27398C0011
6 · The paper itself

Abstract

Macrophage accumulation in the arterial wall and smooth muscle cell (SMC) proliferation are features of type 2 diabetes mellitus (DM) and its vascular complications. However, the effects of diabetic monocyte-derived macrophages on vascular SMC proliferation are not clearly understood. In the present study, we investigated the pro-proliferative effect of macrophages isolated from DM patients on vascular SMCs. Macrophage-conditioned media (MCM) were prepared from macrophages isolated from DM patients. DM-MCM treatment induced HASMC proliferation, decreased p21(Cip1) and p27(Kip1) expressions, and increased microRNA (miR)-17-5p and miR-221 expressions. Inhibition of either miR-17-5p or miR-221 inhibited DM-MCM-induced cell proliferation. Inhibition of miR-17-5p abolished DM-MCM-induced p21(Cip1) down-regulation; and inhibition of miR-221 attenuated the DM-MCM-induced p27(Kip1) down-regulation. Furthermore, blocking assays demonstrated that PDGF-CC in DM-MCM is the major mediators of cell proliferation in SMCs. In conclusion, our present data support the hypothesis that SMC proliferation stimulated by macrophages may play critical roles in vascular complications in DM patients and suggest a new mechanism by which arterial disease is accelerated in diabetes.

Indexed as

AdultAortaBecaplerminCell ProliferationCells, CulturedCulture Media, ConditionedCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Diabetes Mellitus, Type 2Down-RegulationEnzyme-Linked Immunosorbent AssayHumansLymphokinesMacrophagesMicroRNAsMiddle AgedBecaplerminCulture Media, ConditionedCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27LymphokinesMicroRNAsMIR221, humanMIRN17 microRNA, humanOsteopontinPlatelet-Derived Growth Factorplatelet-derived growth factor CProto-Oncogene Proteins c-sis

Identifiers

PMID25409512
PMCPMC4237499
OpenAlexW2036384870

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.