Evidence map›Paper›PMID 8080047›Full record

ArticleThe American journal of pathology1994

Human serum amyloid A genes are expressed in monocyte/macrophage cell lines.

S Urieli-Shoval, R L Meek, R H Hanson, N Eriksen, E P Benditt

Open access · greenAbstract read
In one paragraph

Article in The American journal of pathology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

27 citing papers in PubMed, 91 citations in OpenAlex.

  1. SAA4: An Underdog Within the Serum Amyloid a Superfamily?International journal of molecular sciences · 2026
    Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Amyloid A in Serum and Ascitic Fluid as a Novel Diagnostic Marker of Spontaneous Bacterial Peritonitis.Anti-inflammatory & anti-allergy agents in medicinal chemistry · 2020
    Article
  7. Article
  8. Picroside II Isolated fromMolecules (Basel, Switzerland) · 2019
    Article
  9. Article
  10. Serum Amyloid A1 Is an Epithelial Prorestitutive Factor.The American journal of pathology · 2018
    Article
  11. Article
  12. The cytokine-serum amyloid A-chemokine network.Cytokine & growth factor reviews · 2016
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Expression of serum amyloid a in human ovarian epithelial tumors: implication for a role in ovarian tumorigenesis.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2010
    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

5 authors at 1 institution in 1 country.

S Urieli-ShovalDepartment of Pathology, University of Washington, Seattle 98195.
R L Meek
R H Hanson
N Eriksen
E P Benditt
University of Washington · US

Funding

SPECIALIZED CENTER OF RESEARCH IN ARTERIOSCLEROSISP50HL047151 · NHLBI · UNIVERSITY OF WASHINGTON · PI DEEB, SAMIR · 1992 to 1996
–
SAA LIPOPROTEIN FAMILY--FUNCTION &ROLE IN AMYLOIDOSISR01HL040079 · NHLBI · UNIVERSITY OF WASHINGTON · PI GIACHELLI, CECILIA M. · 1988 to 1997
–
NHLBI NIH HHS HL40079NHLBI NIH HHS HL47151
6 · The paper itself

Abstract

Serum amyloid A (apoSAA) is a family of proteins found, mainly associated with high density lipoproteins, in the blood plasma of mammals and at least one avian species, the Pekin duck. These proteins are present in small amounts under normal circumstances, but their concentration is capable of rising 100- to 1,000-fold in situations involving tissue injury or infection. Like classic acute phase proteins they are produced in the liver; however, expression of one of the apoSAA genes is known to occur in activated macrophages of mice. We examined three human macrophage precursor cell lines (THP-1, U-937, and HL-60), before and after differentiation with phorbol 12-myristate 13-acetate or 1 alpha,25-dihydroxy-vitamin D3, for apoSAA messenger (m)-RNA expression and found that: 1) induction of steady-state apoSAA mRNA by lipopolysaccharide, interleukin-1, or interleukin-6 required the presence of the synthetic glucocorticoid dexamethasone; 2) the three known active genes, apoSAA1, apoSAA2, and apoSAA4, were induced in THP-1 cells, whereas the pseudogene apoSAA3 was not; 3) differentiated and undifferentiated THP-1 cells expressed apoSAA mRNA, but U-937 cells expressed apoSAA mRNA (low levels) only after phorbol 12-myristate 13-acetate differentiation and HL-60 cells did not express apoSAA mRNA whether differentiated or not; 4) apoSAA protein was detectable immunologically at a low level in lyophilized medium from induced THP-1 cells. Our findings are compatible with the hypotheses that 1) apoSAA gene expression in human monocytes/macrophages in vivo is differentiation dependent; 2) activated macrophages provide a local source of apoSAA at sites of tissue injury or inflammation; 3) apoSAA is induced in tissue macrophages by local stimuli, under conditions that may not evoke the systemic acute phase response.

Indexed as

Base SequenceDexamethasoneGene Expression RegulationHumansLeukemiaLipopolysaccharidesLymphomaMacrophagesMolecular Sequence DataMonocytesRNA, MessengerSerum Amyloid A ProteinTime FactorsTumor Cells, CulturedDexamethasoneLipopolysaccharidesRNA, MessengerSerum Amyloid A Protein

Identifiers

PMID8080047
PMCPMC1890325
OpenAlexW2414776223

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.