Evidence map›Paper›PMID 20110337›Full record

ArticleCardiovascular research2010

An angiotensin II- and NF-kappaB-dependent mechanism increases connexin 43 in murine arteries targeted by renin-dependent hypertension.

Florian Alonso, Nathalie Krattinger, Lucia Mazzolai, Alexander Simon, Gérard Waeber, Paolo Meda, Jacques-Antoine Haefliger

Open access · bronzeAbstract read
In one paragraph

Article in Cardiovascular research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

51 citing papers in PubMed, 95 citations in OpenAlex.

  1. Injury-induced connexin 43 expression regulates endothelial wound healing.American journal of physiology. Heart and circulatory physiology · 2025
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  6. The Potential Role of Connexins in the Pathogenesis of Atherosclerosis.International journal of molecular sciences · 2023
    Review
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  8. Article
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  14. Endothelial Connexins in Developmental and Pathological Angiogenesis.Cold Spring Harbor perspectives in medicine · 2022
    Review
  15. Article
  16. Article
  17. Adenovirus targets transcriptional and posttranslational mechanisms to limit gap junction function.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
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  19. Article
  20. Review
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

7 authors at 2 institutions in 1 country.

Florian AlonsoService of Internal Medicine, Laboratory of Experimental Medicine 19-135S, University Hospital, CHUV-1011 Lausanne, Switzerland.
Nathalie Krattinger
Lucia Mazzolai
Alexander Simon
Gérard Waeber
Paolo Meda
Jacques-Antoine Haefliger
University Hospital of Lausanne · CHUniversity of Geneva · CH

Funding

Gap Junction Mediated Signaling and Vascular ResponsesR01HL064232 · NHLBI · UNIVERSITY OF ARIZONA · PI SIMON, ALEXANDER M · 2001 to 2010
$2.2M
NHLBI NIH HHS HL64232NHLBI NIH HHS R01 HL064232
6 · The paper itself

Abstract

aimsConnexins (Cxs) play a role in the contractility of the aorta wall. We investigated how connexins of the endothelial cells (ECs; Cx37, Cx40) and smooth muscle cells (SMCs; Cx43, Cx45) of the aorta change during renin-dependent and -independent hypertension. METHODS AND

resultsWe subjected both wild-type (WT) mice and mice lacking Cx40 (Cx40(-/-)), to either a two-kidney, one-clip procedure or to N-nitro-l-arginine-methyl-ester treatment, which induce renin-dependent and -independent hypertension, respectively. All hypertensive mice featured a thickened aortic wall, increased levels of Cx37 and Cx45 in SMC, and of Cx40 in EC (except in Cx40(-/-) mice). Cx43 was up-regulated, with no effect on its S368 phosphorylation, only in the SMCs of renin-dependent models of hypertension. Blockade of the renin-angiotensin system of Cx40(-/-) mice normalized blood pressure and prevented both aortic thickening and Cx alterations. Ex vivo exposure of WT aortas, carotids, and mesenteric arteries to physiologically relevant levels of angiotensin II (AngII) increased the levels of Cx43, but not of other Cx. In the aortic SMC line of A7r5 cells, AngII activated kinase-dependent pathways and induced binding of the nuclear factor-kappa B (NF-kappaB) to the Cx43 gene promoter, increasing Cx43 expression.

conclusionIn both large and small arteries, hypertension differently regulates Cx expression in SMC and EC layers. Cx43 is selectively increased in renin-dependent hypertension via an AngII activation of the extracellular signal-regulated kinase and NF-kappaB pathways.

Indexed as

Angiotensin-Converting Enzyme InhibitorsAngiotensin IIAngiotensin II Type 1 Receptor BlockersAnimalsAntihypertensive AgentsAortaBinding SitesBlood PressureCarotid ArteriesCell LineConnexin 43ConnexinsDisease Models, AnimalEndothelial CellsExtracellular Signal-Regulated MAP KinasesGap Junction alpha-5 ProteinAngiotensin-Converting Enzyme InhibitorsAngiotensin IIAngiotensin II Type 1 Receptor BlockersAntihypertensive AgentsConnexin 43ConnexinsExtracellular Signal-Regulated MAP KinasesGap Junction alpha-5 ProteinGJA1 protein, mouseNF-kappa BNG-Nitroarginine Methyl EsterRenin

Identifiers

PMID20110337
PMCPMC2883896
OpenAlexW2145418414

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.