Evidence map›Paper›PMID 27105554›Full record

ArticleToxicology and applied pharmacology2016

Mitochondrial-targeted aryl hydrocarbon receptor and the impact of 2,3,7,8-tetrachlorodibenzo-p-dioxin on cellular respiration and the mitochondrial proteome.

Hye Jin Hwang, Peter Dornbos, Michelle Steidemann, Taylor K Dunivin, Mike Rizzo, John J LaPres

Abstract read
In one paragraph

Article in Toxicology and applied pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
6.0field-weighted citation impact, top 4% 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

44 citing papers in PubMed, 77 citations in OpenAlex.

  1. Review
  2. AhR activation inhibits DRP1-induced mitochondrial fission in airway smooth muscle during asthma.American journal of respiratory cell and molecular biology · 2026
    Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Heavy metals, oxidative stress, and the role of AhR signaling.Toxicology and applied pharmacology · 2024
    Review
  10. Article
  11. Intestinal tryptophan metabolism in disease prevention and swine production.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2023
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. The Aryl Hydrocarbon Receptor, Epigenetics and the Aging Process.The journal of nutrition, health & aging · 2023
    Article
  20. The Role of the Kynurenine/AhR Pathway in Diseases Related to Metabolism and Cancer.International journal of tryptophan research : IJTR · 2023
    Review
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

6 authors at 1 institution in 1 country.

Hye Jin HwangDepartment of Biochemistry and Molecular Biology, Michigan State University, East Lansing, MI 48824, United States; Center for Mitochondrial Science and Medicine, Michigan State University, East Lansing, MI 48824, United States.
Peter DornbosDepartment of Biochemistry and Molecular Biology, Michigan State University, East Lansing, MI 48824, United States; Institute for Integrative Toxicology, Michigan State University, East Lansing, MI 48824-1319, United States.
Michelle SteidemannInstitute for Integrative Toxicology, Michigan State University, East Lansing, MI 48824-1319, United States; Department of Pharmacology and Toxicology, Michigan State University, East Lansing, MI 48824, United States.
Taylor K DunivinDepartment of Microbiology and Molecular Genetics, Michigan State University, East Lansing, MI 48824, United States.
Mike RizzoInstitute for Integrative Toxicology, Michigan State University, East Lansing, MI 48824-1319, United States; Cell and Molecular Biology Graduate Program, Michigan State University, East Lansing, MI 48824, United States.
John J LaPresDepartment of Biochemistry and Molecular Biology, Michigan State University, East Lansing, MI 48824, United States; Center for Mitochondrial Science and Medicine, Michigan State University, East Lansing, MI 48824, United States. Electronic address: lapres@msu.edu.
Michigan State University · US

Funding

VOLATILE ORGANIC CONTAMINANTS--QUANTIFYING THEIR MOVEMENT IN THE UNSATURATED ZONEP42ES004911 · NIEHS · MICHIGAN STATE UNIVERSITY · PI Timothy R. Zacharewski · 1989 to 2026
$64.9M
MULTIDISCIPLINARY TRAINING IN ENVIRONMENTAL TOXICOLOGYT32ES007255 · NIEHS · MICHIGAN STATE UNIVERSITY · PI JOHN J LAPRES · 1989 to 2026
$9.3M
NIEHS NIH HHS P42 ES004911NIEHS NIH HHS T32 ES007255
6 · The paper itself

Abstract

The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor within the Per-Arnt-Sim (PAS) domain superfamily. Exposure to the most potent AHR ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), is associated with various pathological effects including metabolic syndrome. While research over the last several years has demonstrated a role for oxidative stress and metabolic dysfunction in AHR-dependent TCDD-induced toxicity, the role of the mitochondria in this process has not been fully explored. Our previous research suggested that a portion of the cellular pool of AHR could be found in the mitochondria (mitoAHR). Using a protease protection assay with digitonin extraction, we have now shown that this mitoAHR is localized to the inter-membrane space (IMS) of the organelle. TCDD exposure induced a degradation of mitoAHR similar to that of cytosolic AHR. Furthermore, siRNA-mediated knockdown revealed that translocase of outer-mitochondrial membrane 20 (TOMM20) was involved in the import of AHR into the mitochondria. In addition, TCDD altered cellular respiration in an AHR-dependent manner to maintain respiratory efficiency as measured by oxygen consumption rate (OCR). Stable isotope labeling by amino acids in cell culture (SILAC) identified a battery of proteins within the mitochondrial proteome influenced by TCDD in an AHR-dependent manner. Among these, 17 proteins with fold changes≥2 are associated with various metabolic pathways, suggesting a role of mitochondrial retrograde signaling in TCDD-mediated pathologies. Collectively, these studies suggest that mitoAHR is localized to the IMS and AHR-dependent TCDD-induced toxicity, including metabolic dysfunction, wasting syndrome, and hepatic steatosis, involves mitochondrial dysfunction.

Indexed as

AnimalsCell Line, TumorCell RespirationHSP90 Heat-Shock ProteinsIntracellular Signaling Peptides and ProteinsMembrane Transport ProteinsMiceMitochondriaMitochondrial Precursor Protein Import Complex ProteinsOxygen ConsumptionPolychlorinated DibenzodioxinsProteomeReceptors, Aryl HydrocarbonReceptors, Cell SurfaceRNA, Small Interferingaryl hydrocarbon receptor-interacting proteinHSP90 Heat-Shock ProteinsIntracellular Signaling Peptides and ProteinsMembrane Transport ProteinsMitochondrial Precursor Protein Import Complex ProteinsPolychlorinated DibenzodioxinsProteomeReceptors, Aryl HydrocarbonReceptors, Cell SurfaceRNA, Small InterferingTomm20 protein, mouse2,3,7,8-Tetrachlorodibenzo-p-dioxin, TCDDAryl hydrocarbon receptorMitochondriaOxidative phosphorylationProteomicsSILAC

Identifiers

PMID27105554
PMCPMC4930739
OpenAlexW2338789091

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.