Evidence map›Paper›PMID 18195103›Full record

ArticleThe Journal of cell biology2008

Prohibitin-1 maintains the angiogenic capacity of endothelial cells by regulating mitochondrial function and senescence.

Michael Schleicher, Benjamin R Shepherd, Yajaira Suarez, Carlos Fernandez-Hernando, Jun Yu, Yong Pan, Lisette M Acevedo, Gerald S Shadel, William C Sessa

Abstract read
In one paragraph

Article in The Journal of cell biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
–field-weighted citation impact
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

99 citing papers in PubMed.

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  15. Article
  16. The Yun/Prohibitin complex regulates adultProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  17. Article
  18. Review
  19. Article
  20. Metabolomics of Multimorbidity: Could It Be theFrontiers in molecular biosciences · 2022
    Article

39 more citing papers are in PubMed but not listed here.

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.

Michael SchleicherDepartment of Pharmacology, and Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT 06536, USA.
Benjamin R Shepherd
Yajaira Suarez
Carlos Fernandez-Hernando
Jun Yu
Yong Pan
Lisette M Acevedo
Gerald S Shadel
William C Sessa

Funding

SOCS-1 and endothelial dysfunction in graft arteriosclerosisP01HL070295 · NHLBI · YALE UNIVERSITY · PI BENDER, JEFFREY R. · 2001 to 2010
$17.9M
PHOSPHORYLATION AND ENDOTHELIAL NITRIC OXIDE PRODUCTIONR01HL064793 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 2000 to 2016
$6.3M
Optimizing Therapeutic Revascularization by Endothelial Cell TransplantationR01HL085416 · NHLBI · YALE UNIVERSITY · PI POBER, JORDAN S, SALTZMAN, W. MARK · 2006 to 2019
$5.9M
Endothelial NOS by Protein-Protein IntractionsR01HL061371 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 1999 to 2008
$3.6M
Mitochondrial Dysfunction and Oxidative Stress in Ataxia TelangiectasiaR01NS056206 · NINDS · YALE UNIVERSITY · PI SHADEL, GERALD · 2007 to 2011
$1.9M
Vascular Remodeling: Role of Nitric OxideR01HL057665 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C. · 1996 to 2004
$1.5M
NHLBI PROTEOMICS INITIATIVE-N01HV28186N01HV028186 · HV · YALE UNIVERSITY · PI WILLIAMS, KENNETH · 2002 to 2006
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NHLBI NIH HHS 1-R01 HL 085416NHLBI NIH HHS N01 HV028186NHLBI NIH HHS N01-HV-28186NHLBI NIH HHS P01 HL070295NHLBI NIH HHS P01 HL 70295NHLBI NIH HHS R01 HL057665NHLBI NIH HHS R01 HL061371NHLBI NIH HHS R01 HL064793NHLBI NIH HHS R01 HL085416NHLBI NIH HHS R01 HL 57665NHLBI NIH HHS R01 HL 61371NHLBI NIH HHS R01 HL64793NINDS NIH HHS R01 NS056206
6 · The paper itself

Abstract

Prohibitin 1 (PHB1) is a highly conserved protein that is mainly localized to the inner mitochondrial membrane and has been implicated in regulating mitochondrial function in yeast. Because mitochondria are emerging as an important regulator of vascular homeostasis, we examined PHB1 function in endothelial cells. PHB1 is highly expressed in the vascular system and knockdown of PHB1 in endothelial cells increases mitochondrial production of reactive oxygen species via inhibition of complex I, which results in cellular senescence. As a direct consequence, both Akt and Rac1 are hyperactivated, leading to cytoskeletal rearrangements and decreased endothelial cell motility, e.g., migration and tube formation. This is also reflected in an in vivo angiogenesis assay, where silencing of PHB1 blocks the formation of functional blood vessels. Collectively, our results provide evidence that PHB1 is important for mitochondrial function and prevents reactive oxygen species-induced senescence and thereby maintains the angiogenic capacity of endothelial cells.

Indexed as

Cellular SenescenceNeovascularization, PhysiologicAnimalsAortaCells, CulturedCytoskeletonElectron Transport Complex IEndothelial CellsEndothelium, VascularHumansMiceMice, Inbred StrainsMitochondriaMitochondrial MembranesNeuropeptidesPhosphatidylinositol 3-KinasesElectron Transport Complex INeuropeptidesPHB protein, humanPhosphatidylinositol 3-KinasesProhibitinsProto-Oncogene Proteins c-aktrac1 GTP-Binding ProteinRac1 protein, mouserac GTP-Binding ProteinsReactive Oxygen SpeciesRepressor Proteins

Identifiers

PMID18195103
PMCPMC2213620

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.