Evidence map›Paper›PMID 25816687›Full record

ArticleAntioxidants & redox signaling2015

Taurine Chloramine Stimulates Efferocytosis Through Upregulation of Nrf2-Mediated Heme Oxygenase-1 Expression in Murine Macrophages: Possible Involvement of Carbon Monoxide.

Wonki Kim, Hoon-Ui Kim, Ha-Na Lee, Seung Hyeon Kim, Chaekyun Kim, Young-Nam Cha, Yeonsoo Joe, Hun Taeg Chung, Jaebong Jang, Kyeojin Kim and 4 more

Abstract read
In one paragraph

Article in Antioxidants & redox signaling, 2015. 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
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

26 citing papers in PubMed, 56 citations in OpenAlex.

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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

14 authors at 4 institutions in 1 country.

Wonki Kim1 Tumor Microenvironment Global Core Research Center and Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University , Seoul, Republic of Korea.
Hoon-Ui Kim1 Tumor Microenvironment Global Core Research Center and Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University , Seoul, Republic of Korea.
Ha-Na Lee1 Tumor Microenvironment Global Core Research Center and Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University , Seoul, Republic of Korea.
Seung Hyeon Kim1 Tumor Microenvironment Global Core Research Center and Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University , Seoul, Republic of Korea.
Chaekyun Kim2 Department of Pharmacology and Toxicology, College of Medicine, Inha University , Incheon, Republic of Korea.
Young-Nam Cha2 Department of Pharmacology and Toxicology, College of Medicine, Inha University , Incheon, Republic of Korea.
Yeonsoo Joe3 Meta-Inflammation Basic Research Laboratory, School of Biological Sciences, University of Ulsan , Ulsan, Republic of Korea.
Hun Taeg Chung3 Meta-Inflammation Basic Research Laboratory, School of Biological Sciences, University of Ulsan , Ulsan, Republic of Korea.
Jaebong Jang1 Tumor Microenvironment Global Core Research Center and Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University , Seoul, Republic of Korea.
Kyeojin Kim1 Tumor Microenvironment Global Core Research Center and Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University , Seoul, Republic of Korea.
Young-Ger Suh1 Tumor Microenvironment Global Core Research Center and Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University , Seoul, Republic of Korea.
Hyeon-Ok Jin4 KIRAMS Radiation Biobank, Korea Institute of Radiological & Medical Sciences , Seoul, Republic of Korea.
Jin Kyung Lee4 KIRAMS Radiation Biobank, Korea Institute of Radiological & Medical Sciences , Seoul, Republic of Korea.
Young-Joon Surh1 Tumor Microenvironment Global Core Research Center and Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University , Seoul, Republic of Korea.
Seoul National University · KRInha University · KRKorea Institute of Radiological and Medical Sciences · KRUniversity of Ulsan · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsTo examine the pro-resolving effects of taurine chloramine (TauCl).

resultsTauCl injected into the peritoneum of mice enhanced the resolution of zymosan A-induced peritonitis. Furthermore, when the macrophages obtained from peritoneal exudates were treated with TauCl, their efferocytic ability was elevated. In the murine macrophage-like RAW264.7 cells exposed to TauCl, the proportion of macrophages engulfing the apoptotic neutrophils was also increased. In these macrophages treated with TauCl, expression of heme oxygenase-1 (HO-1) was elevated along with increased nuclear translocation of the nuclear factor E2-related factor 2 (Nrf2). TauCl binds directly to Kelch-like ECH association protein 1 (Keap1), which appears to retard the Keap1-driven degradation of Nrf2. This results in stabilization and enhanced nuclear translocation of Nrf2 and upregulation of HO-1 expression. TauCl, when treated to peritoneal macrophages isolated from either Nrf2 or HO-1 wild-type mice, stimulated efferocytosis (phagocytic engulfment of apoptotic neutrophils by macrophages), but not in the macrophages from Nrf2 or HO-1 knockout mice. Furthermore, transcriptional expression of some scavenger receptors recognizing the phosphatidylserines exposed on the surface of apoptotic cells was increased in RAW264.7 cells treated with TauCl. Pharmacologic inhibition of HO-1 activity or knockdown of HO-1 gene in RAW264.7 cells abolished the TauCl-induced efferocytosis, whereas both overexpression of HO-1 and treatment with carbon monoxide (CO), the product of HO, potentiated the efferocytic activity of macrophages. INNOVATION: This work provides the first evidence that TauCl stimulates efferocytosis by macrophages. The results of this study suggest the therapeutic potential of TauCl in the management of inflammatory disorders.

conclusionTauCl can facilitate resolution of inflammation by increasing the efferocytic activity of macrophages through Nrf2-mediated HO-1 upregulation and subsequent production of CO.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCarbon MonoxideCytoskeletal ProteinsDisease Models, AnimalHeme Oxygenase-1HumansInflammationJurkat CellsKelch-Like ECH-Associated Protein 1MacrophagesMacrophages, PeritonealMiceNF-E2-Related Factor 2PhagocytosisTaurineAdaptor Proteins, Signal TransducingCarbon MonoxideCytoskeletal ProteinsHeme Oxygenase-1Keap1 protein, mouseKelch-Like ECH-Associated Protein 1N-chlorotaurineNfe2l2 protein, mouseNF-E2-Related Factor 2TaurineZymosan

Identifiers

PMID25816687
PMCPMC4492774
OpenAlexW2315810631

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.