Evidence map›Paper›PMID 27469269›Full record

ArticleTranslational research : the journal of laboratory and clinical medicine2016

Stanniocalcin-1 attenuates ischemic cardiac injury and response of differentiating monocytes/macrophages to inflammatory stimuli.

Arezoo Mohammadipoor, Ryang Hwa Lee, Darwin J Prockop, Thomas J Bartosh

Open access · greenAbstract read
In one paragraph

Article in Translational research : the journal of laboratory and clinical medicine, 2016. 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
3.0field-weighted citation impact, top 9% 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, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Cell Therapies for Acute Radiation Syndrome.International journal of molecular sciences · 2024
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  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

4 authors at 2 institutions in 1 country.

Arezoo MohammadipoorInstitute for Regenerative Medicine, Texas A&M University Health Science Center, College of Medicine, Temple, Tex, USA.
Ryang Hwa LeeInstitute for Regenerative Medicine, Texas A&M University Health Science Center, College of Medicine, Temple, Tex, USA.
Darwin J ProckopInstitute for Regenerative Medicine, Texas A&M University Health Science Center, College of Medicine, Temple, Tex, USA.
Thomas J BartoshInstitute for Regenerative Medicine, Texas A&M University Health Science Center, College of Medicine, Temple, Tex, USA. Electronic address: bartosh@medicine.tamhsc.edu.
Texas A&M University · USTemple College · US

Funding

PREPARATION AND DISTRUBUTION OF ADULT STEM CELLS: HUMAN &RODENTP40RR017447 · NCRR · TULANE UNIVERSITY OF LOUISIANA · PI PROCKOP, DARWIN JOHNSON · 2003 to 2011
$8.9M
Preparation and Distribution of Adult Stem CellsP40OD011050 · OD · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI PROCKOP, DARWIN JOHNSON · 2012 to 2017
$6.0M
Adult Stem Cells for Repair of Cardiac DamageR01HL073755 · NHLBI · TULANE UNIVERSITY OF LOUISIANA · PI PROCKOP, DARWIN JOHNSON · 2003 to 2010
$3.1M
NCRR NIH HHS P40 RR017447NHLBI NIH HHS R01 HL073755NIH HHS P40 OD011050
6 · The paper itself

Abstract

Stanniocalcin-1 (STC-1) is a multifunctional glycoprotein with antioxidant and anti-inflammatory properties. Ischemic myocardial necrosis generates "danger" signals that perpetuate detrimental inflammatory reactions often involving monocyte recruitment and their subsequent differentiation into proinflammatory macrophages. Therefore, we evaluated the effects of recombinant STC-1 (rSTC-1) on monocyte phenotype and in a mouse model of myocardial infarction. Using an established protocol to differentiate human monocytes into macrophages, we demonstrated that rSTC-1 did not alter morphology of the differentiated cells, toll-like receptor (TLR) 4 expression, or expression of the myeloid cell marker CD11b. However, rSTC-1 treatment before differentiation attenuated the rise in the expression of CD14, a TLR4 coreceptor and pathogen sensor that propagates innate immune responses, and suppressed levels of inflammatory cytokines produced by the differentiated cells in response to the CD14-TLR4 ligand lipopolysaccharide. Moreover, rSTC-1 treatment reduced CD14 expression in monocytes stimulated with endogenous danger signals. Interestingly, the effects of rSTC-1 on CD14 expression were not reproduced by a superoxide dismutase mimetic. In mice with induced myocardial infarcts, intravenous administration of rSTC-1 decreased CD14 expression in the heart as well as levels of tumor necrosis factor alpha, C-X-C motif ligand 2, interleukin 1 beta, and myeloperoxidase. It also suppressed the formation of scar tissue while enhancing cardiac function. The data suggests that one of the beneficial effects of STC-1 might be attributed to suppression of CD14 on recruited monocytes and macrophages that limits their inflammatory response. STC-1 may be a promising therapy to protect the heart and other tissues from ischemic injury.

Indexed as

AnimalsBiomarkersCell DifferentiationCell MembraneCicatrixCytokinesGlycoproteinsHeart Function TestsHumansInflammationInflammation MediatorsInjections, IntravenousLipopolysaccharide ReceptorsMacrophagesMaleMice, Inbred NODBiomarkersCytokinesGlycoproteinsInflammation MediatorsLipopolysaccharide ReceptorsRecombinant Proteinsteleocalcin

Identifiers

PMID27469269
PMCPMC5099094
OpenAlexW2466930311

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.