Evidence map›Paper›PMID 29858374›Full record

ArticleDrug metabolism and disposition: the biological fate of chemicals2018

Regulation of Cytosolic Sulfotransferases in Models of Human Hepatocyte Development.

Sarah Dubaisi, Kathleen G Barrett, Hailin Fang, Jorge Guzman-Lepe, Alejandro Soto-Gutierrez, Thomas A Kocarek, Melissa Runge-Morris

Open access · bronzeAbstract read
In one paragraph

Article in Drug metabolism and disposition: the biological fate of chemicals, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.1field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Aha1 Is an Autonomous Chaperone for SULT1A1.Chemical research in toxicology · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Developmental Expression of the Cytosolic Sulfotransferases in Human Liver.Drug metabolism and disposition: the biological fate of chemicals · 2019
    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

7 authors at 2 institutions in 1 country.

Sarah DubaisiDepartment of Pharmacology (S.D.) and Institute of Environmental Health Sciences (K.G.B., H.F., T.A.K., M.R.-M.), Wayne State University, Detroit, Michigan; and Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania (J.G.-L., A.S.-G.).
Kathleen G BarrettDepartment of Pharmacology (S.D.) and Institute of Environmental Health Sciences (K.G.B., H.F., T.A.K., M.R.-M.), Wayne State University, Detroit, Michigan; and Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania (J.G.-L., A.S.-G.).
Hailin FangDepartment of Pharmacology (S.D.) and Institute of Environmental Health Sciences (K.G.B., H.F., T.A.K., M.R.-M.), Wayne State University, Detroit, Michigan; and Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania (J.G.-L., A.S.-G.).
Jorge Guzman-LepeDepartment of Pharmacology (S.D.) and Institute of Environmental Health Sciences (K.G.B., H.F., T.A.K., M.R.-M.), Wayne State University, Detroit, Michigan; and Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania (J.G.-L., A.S.-G.).
Alejandro Soto-GutierrezDepartment of Pharmacology (S.D.) and Institute of Environmental Health Sciences (K.G.B., H.F., T.A.K., M.R.-M.), Wayne State University, Detroit, Michigan; and Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania (J.G.-L., A.S.-G.).
Thomas A KocarekDepartment of Pharmacology (S.D.) and Institute of Environmental Health Sciences (K.G.B., H.F., T.A.K., M.R.-M.), Wayne State University, Detroit, Michigan; and Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania (J.G.-L., A.S.-G.).
Melissa Runge-MorrisDepartment of Pharmacology (S.D.) and Institute of Environmental Health Sciences (K.G.B., H.F., T.A.K., M.R.-M.), Wayne State University, Detroit, Michigan; and Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania (J.G.-L., A.S.-G.) m.runge-morris@wayne.edu.
University of Pittsburgh · USWayne State University · US

Funding

Pilot Project ProgramP30ES020957 · NIEHS · WAYNE STATE UNIVERSITY · PI RUNGE-MORRIS, MELISSA A · 2014 to 2021
$10.1M
Expression, Regulation and Function of the SULT1C Carcinogen-Activating EnzymesR01ES022606 · NIEHS · WAYNE STATE UNIVERSITY · PI RUNGE-MORRIS, MELISSA A · 2014 to 2025
$4.8M
Mini-Livers Derived from Human IPS Cells for Modeling Steatosis and TherapyR01DK099257 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI NAGRATH, DEEPAK, SOTO-GUTIERREZ, ALEJANDRO · 2014 to 2024
$3.4M
REGULATION OF B CELL SIGNALING BY SHPTP-1R01CA066600 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI NEEL, BENJAMIN G. · 1996 to 2000
$232k
NCI NIH HHS N02 CB066600NIDDK NIH HHS R01 DK099257NIEHS NIH HHS P30 ES020957NIEHS NIH HHS R01 ES022606
6 · The paper itself

Abstract

Cytosolic sulfotransferases (SULTs) are expressed during early life and therefore metabolize endogenous and xenobiotic chemicals during development. Little is currently known about the regulation of individual SULTs in the developing human liver. We characterized SULT expression in primary cultures of human fetal hepatocytes and the HepaRG model of liver cell differentiation. SULT1A1 (transcript variants 1-4), SULT1C2, SULT1C4, SULT1E1, and SULT2A1 were the most abundant transcripts in human fetal hepatocytes. In HepaRG cells, SULT1B1, SULT1C2/3/4, and SULT1E1 mRNA levels increased during the transition from proliferation to confluency and then decreased as the cells underwent further differentiation. By contrast, SULT2A1 mRNA levels increased during differentiation, whereas SULT1A1 and SULT2B1 mRNA levels remained relatively constant. The temporal patterns of SULT1C2, SULT1E1, and SULT2A1 protein content were consistent with those observed at the mRNA level. To identify regulators of SULT expression, cultured fetal hepatocytes and HepaRG cells were treated with a panel of lipid- and xenobiotic-sensing receptor activators. The following effects were observed in both fetal hepatocytes and HepaRG cells: 1) liver X receptor activator treatment increased SULT1A1 transcript variant 5 levels; 2) vitamin D receptor activator treatment increased SULT1C2 and SULT2B1 mRNA levels; and 3) farnesoid X receptor activator treatment decreased SULT2A1 expression. Activators of aryl hydrocarbon receptor, constitutive androstane receptor, pregnane X receptor, and peroxisome proliferator-activated receptors produced additional gene-dependent effects on SULT expression in HepaRG cells. These findings suggest that SULT-regulating chemicals have the potential to modulate physiologic processes and susceptibility to xenobiotic stressors in the developing human liver.

Indexed as

Cell DifferentiationCells, CulturedCytosolFetusHepatocytesHumansLiverRNA, MessengerSulfotransferasesXenobioticsRNA, MessengerSulfotransferasesXenobiotics

Identifiers

PMID29858374
PMCPMC6038032
OpenAlexW2806423640

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.