Evidence map›Paper›PMID 29059213›Full record

ArticlePloS one2017

Endothelial CaMKII as a regulator of eNOS activity and NO-mediated vasoreactivity.

Shubha Murthy, Olha M Koval, Juan M Ramiro Diaz, Santosh Kumar, Daniel Nuno, Jason A Scott, Chantal Allamargot, Linda J Zhu, Kim Broadhurst, Velarchana Santhana and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 42 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Nitric oxide contributes to rapid sclerostin protein loss following mechanical load.Biochemical and biophysical research communications · 2024
    Article
  5. Review
  6. Cardiovascular dysfunction induced by combined exposure to nicotine inhalation and high-fat diet.American journal of physiology. Heart and circulatory physiology · 2024
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. CaMKIIδ Splice Variants in the Healthy and Diseased Heart.Frontiers in cell and developmental biology · 2021
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. The Intrinsic Virtues of EGCG, anMolecules (Basel, Switzerland) · 2020
    Review
  18. Article
  19. 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

14 authors at 2 institutions in 1 country.

Shubha MurthyDepartment of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, Iowa, United States of America.
Olha M KovalDepartment of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, Iowa, United States of America.
Juan M Ramiro DiazDepartment of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, Iowa, United States of America.
Santosh KumarDepartment of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, Iowa, United States of America.
Daniel NunoDepartment of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, Iowa, United States of America.
Jason A ScottDepartment of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, Iowa, United States of America.
Chantal AllamargotCentral Microscopy Research Facility, Office of Vice President of Research and Economic Development, University of Iowa, Iowa City, Iowa, United States of America.
Linda J ZhuDepartment of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, Iowa, United States of America.
Kim BroadhurstDepartment of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, Iowa, United States of America.
Velarchana SanthanaDepartment of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, Iowa, United States of America.
William J KutschkeDepartment of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, Iowa, United States of America.
Kaikobad IraniDepartment of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, Iowa, United States of America.
Kathryn G LampingDepartment of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, Iowa, United States of America.
Isabella M GrumbachDepartment of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, Iowa, United States of America.
University of Iowa · USIowa City VA Health Care System · US

Funding

Mitochondrial CaMKII drives smooth muscle migration and neointimal hyperplasiaR01HL108932 · NHLBI · UNIVERSITY OF IOWA · PI GRUMBACH, ISABELLA MARIA · 2012 to 2021
$3.6M
Mitochondrial CAMKII in smooth muscle as key regulator of hypertension and vascular remodelingI01BX000163 · VA · OKLAHOMA CITY VA MEDICAL CENTER · PI Isabella Maria Grumbach · 2011 to 2026
–
BLRD VA I01 BX000163BLRD VA I01 BX000543BLRD VA I01 BX002940NHLBI NIH HHS R01 HL108932RRD VA I21 RX001561
6 · The paper itself

Abstract

The multifunctional Ca2+/calmodulin-dependent protein kinase II (CaMKII) is a serine/threonine kinase important in transducing intracellular Ca2+ signals. While in vitro data regarding the role of CaMKII in the regulation of endothelial nitric oxide synthase (eNOS) are contradictory, its role in endothelial function in vivo remains unknown. Using two novel transgenic models to express CaMKII inhibitor peptides selectively in endothelium, we examined the effect of CaMKII on eNOS activation, NO production, vasomotor tone and blood pressure. Under baseline conditions, CaMKII activation was low in the aortic wall. Consistently, systolic and diastolic blood pressure, heart rate and plasma NO levels were unaltered by endothelial CaMKII inhibition. Moreover, endothelial CaMKII inhibition had no significant effect on NO-dependent vasodilation. These results were confirmed in studies of aortic rings transduced with adenovirus expressing a CaMKII inhibitor peptide. In cultured endothelial cells, bradykinin treatment produced the anticipated rapid influx of Ca2+ and transient CaMKII and eNOS activation, whereas CaMKII inhibition blocked eNOS phosphorylation on Ser-1179 and dephosphorylation at Thr-497. Ca2+/CaM binding to eNOS and resultant NO production in vitro were decreased under CaMKII inhibition. Our results demonstrate that CaMKII plays an important role in transient bradykinin-driven eNOS activation in vitro, but does not regulate NO production, vasorelaxation or blood pressure in vivo under baseline conditions.

Indexed as

AnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Cell LineHumansNitric OxideNitric Oxide Synthase Type IIIPhosphorylationCalcium-Calmodulin-Dependent Protein Kinase Type 2Nitric OxideNitric Oxide Synthase Type III

Identifiers

PMID29059213
PMCPMC5653296
OpenAlexW2765404685

What OpenQuestion holds

Textmetadata
LicenceCC0
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.