Evidence map›Paper›PMID 25550207›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2015

Syndecan-1 modulates the motility and resolution responses of macrophages.

Julianty Angsana, Jiaxuan Chen, Sumona Smith, Jiantao Xiao, Jing Wen, Liying Liu, Carolyn A Haller, Elliot L Chaikof

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

34 citing papers in PubMed, 51 citations in OpenAlex.

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  5. SDC1 is a critical transmembrane proteoglycan in breast cancer.World journal of surgical oncology · 2025
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  12. Inflammation in the early phase after kidney transplantation is associated with increased long-term all-cause mortality.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2022
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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

8 authors at 2 institutions in 1 country.

Julianty AngsanaFrom the Department of Bioengineering, Georgia Institute of Technology, Atlanta (J.A.); Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA (J.C., L.L., C.A.H., E.L.C.); Department of Surgery, Emory University, Atlanta, GA (S.S., J.X., J.W.); and Wyss Institute of Biologically Inspired Engineering, Harvard University, Boston, MA (E.L.C.).
Jiaxuan ChenFrom the Department of Bioengineering, Georgia Institute of Technology, Atlanta (J.A.); Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA (J.C., L.L., C.A.H., E.L.C.); Department of Surgery, Emory University, Atlanta, GA (S.S., J.X., J.W.); and Wyss Institute of Biologically Inspired Engineering, Harvard University, Boston, MA (E.L.C.).
Sumona SmithFrom the Department of Bioengineering, Georgia Institute of Technology, Atlanta (J.A.); Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA (J.C., L.L., C.A.H., E.L.C.); Department of Surgery, Emory University, Atlanta, GA (S.S., J.X., J.W.); and Wyss Institute of Biologically Inspired Engineering, Harvard University, Boston, MA (E.L.C.).
Jiantao XiaoFrom the Department of Bioengineering, Georgia Institute of Technology, Atlanta (J.A.); Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA (J.C., L.L., C.A.H., E.L.C.); Department of Surgery, Emory University, Atlanta, GA (S.S., J.X., J.W.); and Wyss Institute of Biologically Inspired Engineering, Harvard University, Boston, MA (E.L.C.).
Jing WenFrom the Department of Bioengineering, Georgia Institute of Technology, Atlanta (J.A.); Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA (J.C., L.L., C.A.H., E.L.C.); Department of Surgery, Emory University, Atlanta, GA (S.S., J.X., J.W.); and Wyss Institute of Biologically Inspired Engineering, Harvard University, Boston, MA (E.L.C.).
Liying LiuFrom the Department of Bioengineering, Georgia Institute of Technology, Atlanta (J.A.); Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA (J.C., L.L., C.A.H., E.L.C.); Department of Surgery, Emory University, Atlanta, GA (S.S., J.X., J.W.); and Wyss Institute of Biologically Inspired Engineering, Harvard University, Boston, MA (E.L.C.).
Carolyn A HallerFrom the Department of Bioengineering, Georgia Institute of Technology, Atlanta (J.A.); Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA (J.C., L.L., C.A.H., E.L.C.); Department of Surgery, Emory University, Atlanta, GA (S.S., J.X., J.W.); and Wyss Institute of Biologically Inspired Engineering, Harvard University, Boston, MA (E.L.C.). echaikof@bidmc.harvard.edu challer@bidmc.harvard.edu.
Elliot L ChaikofFrom the Department of Bioengineering, Georgia Institute of Technology, Atlanta (J.A.); Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA (J.C., L.L., C.A.H., E.L.C.); Department of Surgery, Emory University, Atlanta, GA (S.S., J.X., J.W.); and Wyss Institute of Biologically Inspired Engineering, Harvard University, Boston, MA (E.L.C.). echaikof@bidmc.harvard.edu challer@bidmc.harvard.edu.
Emory University · USGeorgia Institute of Technology · US

Funding

Syndecan Shedding in Vascular Lesion FormationR01HL060903 · NHLBI · EMORY UNIVERSITY · PI CHAIKOF, ELLIOT · 1998 to 2012
$3.2M
NHLBI NIH HHS HL060903NHLBI NIH HHS R01 HL060903
6 · The paper itself

Abstract

objectiveSyndecan-1 (Sdc-1) is a member of a family of cell surface proteoglycans, which has been reported to participate in the regulation of events relevant to tissue repair and chronic injury responses, including cell-substrate interactions, matrix remodeling, and cell migration. In this study, we report the functional significance of Sdc-1 in polarized macrophage populations and its role in adhesion and motility events relevant to resolution of the inflammatory program. APPROACH AND

resultsMacrophage Sdc-1 expression is associated with differentiated M2 macrophages with high intrinsic motility, and Sdc-1 deficiency is characterized by impaired migration and enhanced adhesion. Leukocyte infiltration and emigration were examined in a thioglycollate-induced model of peritonitis in Sdc-1(+/+) and Sdc-1(-/-) mice. Although the infiltration of inflammatory cells was similar in both cohorts, a significant delay in the lymphatic clearance of Sdc-1(-/-) macrophages was observed. Moreover, we observed enhanced inflammation and greater burden of atherosclerotic plaques in ApoE(-/-)Sdc-1(-/-) mice maintained on a Western diet.

conclusionsThese results demonstrate that defective motility in Sdc-1(-/-) macrophages promotes a persistent inflammatory state with relevance to the pathogenesis of atherosclerosis.

Indexed as

ChemotaxisAnimalsApolipoproteins EAtherosclerosisCell AdhesionCell DifferentiationCell Line, TumorChemotaxis, LeukocyteCulture Media, ConditionedDiet, High-FatDisease Models, AnimalHumansMacrophages, PeritonealMaleMice, Inbred C57BLMice, KnockoutApolipoproteins ECulture Media, ConditionedSdc1 protein, mouseSyndecan-1cell movementmacrophagesyndecan-1

Identifiers

PMID25550207
PMCPMC4304980
OpenAlexW2162424361

What OpenQuestion holds

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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.