Evidence map›Paper›PMID 22807450›Full record

ArticleThe Journal of biological chemistry2012

α(1)-Acid glycoprotein up-regulates CD163 via TLR4/CD14 protein pathway: possible protection against hemolysis-induced oxidative stress.

Hisakazu Komori, Hiroshi Watanabe, Tsuyoshi Shuto, Azusa Kodama, Hitoshi Maeda, Kenji Watanabe, Hirofumi Kai, Masaki Otagiri, Toru Maruyama

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

25 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
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  3. Article
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  5. Article
  6. Review
  7. Article
  8. An acute phase protein αScientific reports · 2021
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  11. αKidney360 · 2020
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  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
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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 at 3 institutions in 1 country.

Hisakazu KomoriDepartment of Biopharmaceutics, Graduate School of Pharmaceutical Sciences, Kumamoto University, 5-1 Oe-honmachi, Kumamoto 862-0973, Japan.
Hiroshi Watanabe
Tsuyoshi Shuto
Azusa Kodama
Hitoshi Maeda
Kenji Watanabe
Hirofumi Kai
Masaki Otagiri
Toru Maruyama
Kumamoto University · JPJapan Society for the Promotion of Science · JPSojo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD163, a scavenger receptor that is expressed at high levels in the monocyte-macrophage system, is a critical factor for the efficient extracellular hemoglobin (Hb) clearance during hemolysis. Because of the enormous detrimental effect of liberated Hb on our body by its ability to induce pro-inflammatory signals and tissue damage, an understanding of the molecular mechanisms associated with CD163 expression during the acute phase response is a central issue. We report here that α(1)-acid glycoprotein (AGP), an acute phase protein, the serum concentration of which is elevated under various inflammatory conditions, including hemolysis, up-regulates CD163 expression in both macrophage-like differentiated THP-1 (dTHP-1) cells and peripheral blood mononuclear cells in a time- and concentration-dependent manner. Moreover, the subsequent induction of Hb uptake was also observed in AGP-treated dTHP-1 cells. Among representative acute phase proteins such as AGP, α(1)-antitrypsin, C-reactive protein, and haptoglobin, only AGP increased CD163 expression, suggesting that AGP plays a specific role in the regulation of CD163. Consistently, the physiological concentrations of AGP induced CD163, and the subsequent induction of Hb uptake as well as the reduction of oxidative stress in plasma were observed in phenylhydrazine-induced hemolytic model mice, confirming the in vivo role of AGP. Finally, AGP signaling through the toll-like receptor-4 (TLR4) and CD14, the common innate immune receptor complex that normally recognizes bacterial components, was identified as a crucial stimulus that induces the autocrine regulatory loops of IL-6 and/or IL-10 via NF-κB, p38, and JNK pathways, which leads to an enhancement in CD163 expression. These findings provide possible insights into how AGP exerts anti-inflammatory properties against hemolysis-induced oxidative stress.

Indexed as

HemolysisMAP Kinase Signaling SystemOxidative StressUp-RegulationAnimalsAntigens, CDAntigens, Differentiation, MyelomonocyticCD163 AntigenCell Line, TumorC-Reactive ProteinDisease Models, AnimalHaptoglobinsHemoglobinsHumansInterleukin-10Interleukin-6Antigens, CDAntigens, Differentiation, MyelomonocyticCD163 AntigenC-Reactive ProteinHaptoglobinsHemoglobinsIL10 protein, humanIL6 protein, humanInterleukin-10Interleukin-6Lipopolysaccharide ReceptorsMAP Kinase Kinase 4NF-kappa BOrosomucoidp38 Mitogen-Activated Protein KinasesReceptors, Cell SurfaceTLR4 protein, humanTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID22807450
PMCPMC3436313
OpenAlexW2065324814

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.