Evidence map›Paper›PMID 18405916›Full record

ArticleJournal of molecular and cellular cardiology2008

Involvement of connexin 43 in angiotensin II-induced migration and proliferation of saphenous vein smooth muscle cells via the MAPK-AP-1 signaling pathway.

Guanghong Jia, Gang Cheng, Deepak M Gangahar, Devendra K Agrawal

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

26 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Limitations of Current Therapies and Barriers in Alzheimer's Disease.Archives of internal medicine research · 2026
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  9. Upregulation of ATFrontiers in physiology · 2018
    Article
  10. Article
  11. Decreased Expression of Connexin 43 Blunts the Progression of Experimental GN.Journal of the American Society of Nephrology : JASN · 2017
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Role of matrix Gla protein in angiotensin II-induced exacerbation of vascular calcification.American journal of physiology. Heart and circulatory physiology · 2012
    Article
  20. Article
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

4 authors at 2 institutions in 1 country.

Guanghong JiaDepartment of Biomedical Sciences, Creighton University School of Medicine, Omaha, NE 68178, USA.
Gang Cheng
Deepak M Gangahar
Devendra K Agrawal
Creighton University · USCHI Health Nebraska Heart · US

Funding

APOPTOSIS OF SMOOTH MUSCLE CELLS IN CAROTID PLAQUESR01HL073349 · NHLBI · CREIGHTON UNIVERSITY · PI AGRAWAL, DEVENDRA K. · 2004 to 2013
$2.6M
SMOOTH MUSCLE CELL PROLIFERATION IN HUMAN CORONARY ARTERY BYPASS GRAFTSR01HL090580 · NHLBI · CREIGHTON UNIVERSITY · PI AGRAWAL, DEVENDRA K. · 2009 to 2012
$1.4M
FLT3-LIGAND, IMMUNOMODULATION AND THERAPY IN ASTHMAR01HL070885 · NHLBI · CREIGHTON UNIVERSITY · PI AGRAWAL, DEVENDRA K. · 2004 to 2008
$1.1M
NHLBI NIH HHS R01 HL070885NHLBI NIH HHS R01HL070885NHLBI NIH HHS R01 HL073349NHLBI NIH HHS R01HL073349NHLBI NIH HHS R01 HL090580
6 · The paper itself

Abstract

Proliferation and migration of vascular smooth muscle cells (VSMCs) lead to intimal thickening and influence the long-term patency of venous graft post coronary arterial bypass graft. There is increasing evidence that connexins are involved in the development of intimal hyperplasia and restenosis. We assessed connexin 43 (Cx43) expression and its role in angiotensin II-induced proliferation and migration of smooth muscle cells and the signal pathways involved in human saphenous vein bypass conduits. Angiotensin II significantly increased gap junctional intercellular communication and induced the expression of Cx43 in human saphenous vein SMCs in a dose- and time-dependent manner through angiotensin II type 1 receptor. The effect of angiotensin II was blocked by siRNA of ERK 1/2, p38 MAPK and JNK, respectively. Overexpression of Cx43 markedly increased the proliferation of saphenous vein SMCs. However, siRNA for Cx43 inhibited angiotensin II-induced proliferation, cyclin E expression and migration of human saphenous vein SMCs. In dual-luciferase reporter assay, angiotensin II markedly activated AP-1 transcription factor, which was significantly attenuated by a dominant-negative AP-1 (A-Fos) with subsequent inhibition of angiotensin II-induced transcriptional expression of Cx43. These data demonstrate the role of Cx43 in the proliferation and migration of human saphenous vein SMCs and angiotensin II-induced Cx43 expression via mitogen-activated protein kinases (MAPK)-AP-1 signaling pathway.

Indexed as

AgedAngiotensin IICell CommunicationCell MovementCell ProliferationConnexin 43Enzyme ActivationGap JunctionsHumansJNK Mitogen-Activated Protein KinasesMAP Kinase Signaling SystemMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Myocytes, Smooth Musclep38 Mitogen-Activated Protein KinasesReceptor, Angiotensin, Type 1Angiotensin IIConnexin 43JNK Mitogen-Activated Protein KinasesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3p38 Mitogen-Activated Protein KinasesReceptor, Angiotensin, Type 1RNA, Small InterferingTranscription Factor AP-1

Identifiers

PMID18405916
PMCPMC2765202
OpenAlexW1988539866

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.