Evidence map›Paper›PMID 7635951›Full record

ArticleThe Journal of clinical investigation1995

Sickle erythrocytes, after sickling, regulate the expression of the endothelin-1 gene and protein in human endothelial cells in culture.

M Phelan, S P Perrine, M Brauer, D V Faller

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 110 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Magnesium homeostasis in deoxygenated sickle erythrocytes is modulated by endothelin-1 via NaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Red Blood Cells: Chasing Interactions.Frontiers in physiology · 2019
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Endothelin.Pharmacological reviews · 2016
    Review
  17. Article
  18. Article
  19. Review
  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 1 institution in 1 country.

M PhelanCancer Research Center, Boston University Medical Center, Massachusetts 02118, USA.
S P Perrine
M Brauer
D V Faller
Boston University · US

Funding

TREATMENT OF SICKLE CELL ANEMIAP60HL015157 · NHLBI · BOSTON MEDICAL CENTER · PI MCMAHON, LILLIAN E · 1985 to 2002
$5.4M
BIOLOGY OF THE GLOBIN SWITCHR01HL037118 · NHLBI · CHILDREN'S HOSPITAL &RES CTR AT OAKLAND · PI PERRINE, SUSAN P · 1988 to 1994
–
MECHANISMS OF VASOOCCLUSION IN SICKLE CELL ANEMIAR01HL045940 · NHLBI · DANA-FARBER CANCER INSTITUTE · PI FALLER, DOUGLAS V · 1990 to 1994
–
BIOLOGY OF THE FETAL GLOBIN SWITCHR23HL037118 · NHLBI · CHILDREN'S HOSPITAL &RES CTR AT OAKLAND · PI PERRINE, SUSAN P · 1985 to 1987
–
NHLBI NIH HHS HL-15157NHLBI NIH HHS HL-37118NHLBI NIH HHS HL-45940
6 · The paper itself

Abstract

The molecular defect in sickle cell disease resides in the beta globin gene, with consequent defects in erythrocytes only, suggesting that the vascular occlusion and vasomotor instability which characterize this disease are the result of interactions between abnormal sickle erythrocytes and cells of the blood vessel wall. We explored whether sickle erythrocytes may have effects on vascular tone, exclusive of adhesion events. Exposure of human endothelial cells in culture to previously sickled sickle erythrocytes resulted in a four to eight-fold transcriptional induction of the gene encoding the potent vasoconstrictor endothelin-1 (ET-1). Unsickled sickle erythrocytes or normal erythrocytes exposed to "sickling" conditions had no effect on ET-1 gene induction. Contact of the sickled erythrocytes with the endothelium was not required. Elevations in the ET-1 transcript peaked at 3 h after exposure and persisted for up to 24 h. Four to sixfold increases in the amount of ET-1 peptide was released into the medium surrounding the endothelial cells after exposure to sickled sickle erythrocytes. This is the first demonstration of the regulation of gene expression in endothelial cells as a result of interaction with sickle cells, with induction of genes encoding vasoconstrictors. Furthermore, these findings suggest that sickle erythrocytes may have the capacity to affect local vasomotor tone directly.

Indexed as

Cell HypoxiaGene Expression RegulationAnemia, Sickle CellCells, CulturedEndothelin-1EndothelinsEndothelium, VascularErythrocytes, AbnormalHumansProtein PrecursorsRNA, MessengerTranscriptional ActivationUmbilical VeinsVasoconstrictionEndothelin-1EndothelinsProtein PrecursorsRNA, Messenger

Identifiers

PMID7635951
PMCPMC185305
OpenAlexW2033664198

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.