Evidence map›Paper›PMID 30739581›Full record

ArticleCirculation research2019

Novel Paracrine Functions of Smooth Muscle Cells in Supporting Endothelial Regeneration Following Arterial Injury.

Jun Ren, Ting Zhou, Vijaya Satish Sekhar Pilli, Noel Phan, Qiwei Wang, Kartik Gupta, Zhenjie Liu, Nader Sheibani, Bo Liu

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Circulation research, 2019. 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
1.8field-weighted citation impact, top 13% 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, 47 citations in OpenAlex.

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  11. PKCδ regulates the vascular biology in diabetic atherosclerosis.Cell communication and signaling : CCS · 2023
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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

9 authors at 2 institutions in 2 countries.

Jun RenFrom the Division of Vascular Surgery, Department of Surgery, University of Wisconsin-Madison (J.R., T.Z., V.S.S.P., N.P., Q.W., K.G., Z.L., B.L.).
Ting ZhouFrom the Division of Vascular Surgery, Department of Surgery, University of Wisconsin-Madison (J.R., T.Z., V.S.S.P., N.P., Q.W., K.G., Z.L., B.L.).
Vijaya Satish Sekhar PilliFrom the Division of Vascular Surgery, Department of Surgery, University of Wisconsin-Madison (J.R., T.Z., V.S.S.P., N.P., Q.W., K.G., Z.L., B.L.).
Noel PhanFrom the Division of Vascular Surgery, Department of Surgery, University of Wisconsin-Madison (J.R., T.Z., V.S.S.P., N.P., Q.W., K.G., Z.L., B.L.).
Qiwei WangFrom the Division of Vascular Surgery, Department of Surgery, University of Wisconsin-Madison (J.R., T.Z., V.S.S.P., N.P., Q.W., K.G., Z.L., B.L.).
Kartik GuptaFrom the Division of Vascular Surgery, Department of Surgery, University of Wisconsin-Madison (J.R., T.Z., V.S.S.P., N.P., Q.W., K.G., Z.L., B.L.).
Zhenjie LiuFrom the Division of Vascular Surgery, Department of Surgery, University of Wisconsin-Madison (J.R., T.Z., V.S.S.P., N.P., Q.W., K.G., Z.L., B.L.).
Nader SheibaniDepartment of Ophthalmology and Visual Sciences, University of Wisconsin-Madison (N.S.).
Bo LiuFrom the Division of Vascular Surgery, Department of Surgery, University of Wisconsin-Madison (J.R., T.Z., V.S.S.P., N.P., Q.W., K.G., Z.L., B.L.).
University of Wisconsin–Madison · USZhejiang University · CN

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI AMY TRENTHAM-DIETZ · 1985 to 2026
$142.6M
UW Vision Research Core - Administrative CoreP30EY016665 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI ROBERT W NICKELLS · 2005 to 2026
$12.6M
Novel Antiangiogenic Peptides for Treatment of Exudative AMDR24EY022883 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI SHEIBANI, NADER · 2013 to 2017
$6.2M
Molecular Mechanisms in Abdominal Aortic AneuysmR01HL088447 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI LIU, BO · 2011 to 2020
$3.8M
Investigating oxygen metabolism in diabetic retinopathyR01EY026078 · NEI · NORTHWESTERN UNIVERSITY · PI SHEIBANI, NADER, ZHANG, HAO F · 2016 to 2020
$2.3M
Vascular smooth muscle cell apoptosis in intimal hyperplasiaR01HL122562 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI LIU, BO · 2015 to 2018
$1.6M
PKC-Delta in Intimal Hyperplasia after Vascular BypassR01HL081424 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI LIU, BO · 2005 to 2008
$1.6M
NCI NIH HHS P30 CA014520NEI NIH HHS P30 EY016665NEI NIH HHS R01 EY026078NEI NIH HHS R24 EY022883NHLBI NIH HHS R01 HL081424NHLBI NIH HHS R01 HL088447NHLBI NIH HHS R01 HL122562
6 · The paper itself

Abstract

rationaleRegeneration of denuded or injured endothelium is an important component of vascular injury response. Cell-cell communication between endothelial cells and smooth muscle cells (SMCs) plays a critical role not only in vascular homeostasis but also in disease. We have previously demonstrated that PKCδ (protein kinase C-delta) regulates multiple components of vascular injury response including apoptosis of SMCs and production of chemokines, thus is an attractive candidate for a role in SMC-endothelial cells communication.

objectiveTo test whether PKCδ-mediated paracrine functions of SMCs influence reendothelialization in rodent models of arterial injury. METHODS AND

resultsFemoral artery wire injury was performed in SMC-conditional Prkcd knockout mice, and carotid angioplasty was conducted in rats receiving transient Prkcd knockdown or overexpression. SMC-specific knockout of Prkcd impaired reendothelialization, reflected by a smaller Evans blue-excluding area in the knockout compared with the wild-type controls. A similar impediment to reendothelialization was observed in rats with SMC-specific knockdown of Prkcd. In contrast, SMC-specific gene transfer of Prkcd accelerated reendothelialization. In vitro, medium conditioned by AdPKCδ-infected SMCs increased endothelial wound closure without affecting their proliferation. A polymerase chain reaction-based array analysis identified Cxcl1 and Cxcl7 among others as PKCδ-mediated chemokines produced by SMCs. Mechanistically, we postulated that PKCδ regulates Cxcl7 expression through STAT3 (signal transducer and activator of transcription 3) as knockdown of STAT3 abolished Cxcl7 expression. The role of CXCL7 in SMC-endothelial cells communication was demonstrated by blocking CXCL7 or its receptor CXCR2, both significantly inhibited endothelial wound closure. Furthermore, insertion of a Cxcl7 cDNA in the lentiviral vector that carries a Prkcd shRNA overcame the adverse effects of Prkcd knockdown on reendothelialization.

conclusionsSMCs promote reendothelialization in a PKCδ-dependent paracrine mechanism, likely through CXCL7-mediated recruitment of endothelial cells from uninjured endothelium.

Indexed as

AnimalsApoptosisCarotid Artery InjuriesChemokine CXCL1ChemokinesChemokines, CXCEndothelial CellsFemoral ArteryGene Knockout TechniquesMiceMice, TransgenicMyocytes, Smooth MuscleParacrine CommunicationProtein Kinase C-deltaReceptors, Interleukin-8BRegenerationChemokine CXCL1ChemokinesChemokines, CXCCxcl1 protein, ratCxcr2 protein, ratPpbp protein, ratProtein Kinase C-deltaReceptors, Interleukin-8BStat3 protein, ratSTAT3 Transcription Factorchemokines, CXCendothelial cellsmuscle, smoothprotein kinase C-deltaregenerationSTAT3 transcription factor

Identifiers

PMID30739581
PMCPMC6459708
OpenAlexW2913592557

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.