Evidence map›Paper›PMID 18468591›Full record

ArticleChemico-biological interactions2008

Preservation of hepatic phenotype in lentiviral-transduced primary human hepatocytes.

Stephanie M Zamule, Stephen C Strom, Curtis J Omiecinski

Open access · greenAbstract read
In one paragraph

Article in Chemico-biological interactions, 2008. 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
0.8field-weighted citation impact, top 27% 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, 25 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

3 authors at 2 institutions in 1 country.

Stephanie M ZamuleCenter for Molecular Toxicology & Carcinogenesis and Department of Veterinary & Biomedical Sciences, Pennsylvania State University, 101 Life Sciences Building, University Park, PA 16802, USA.
Stephen C Strom
Curtis J Omiecinski
Pennsylvania State University · USUniversity of Pittsburgh · US

Funding

WILDLIFE BIOMARKER APPLICATIONS TO REMEDIATION DECISION MAKINGP42ES004696 · NIEHS · UNIVERSITY OF WASHINGTON · PI GALLAGHER, EVAN P · 1987 to 2021
$51.2M
Targeting Dynamics of CAR and PXR in the Mouse and Human GenomesR01GM066411 · NIGMS · PENNSYLVANIA STATE UNIVERSITY-UNIV PARK · PI OMIECINSKI, CURTIS J · 2002 to 2017
$4.5M
NIEHS NIH HHS P42 ES004696NIGMS NIH HHS GM066411NIGMS NIH HHS R01 GM066411
6 · The paper itself

Abstract

Lentiviral vectors effectively transduce both dividing and non-dividing cells and stably integrate into the genome of the host cell. In this study, we evaluated the usefulness of a lentiviral system for genetic modulation of primary human hepatocyte cultures. Infection with GFP-expressing lentivectors shows that Huh7 and HepG2 cell lines, as well as primary cultures of human hepatocytes, are efficiently transduced by lentiviral vectors. Real-time RT-PCR analyses demonstrate that infection with lentivectors does not alter hepatic hallmarks such as the expression of the nuclear receptors CAR, PXR, RXR alpha, or HNF4 alpha, or expression of the secretory protein, albumin. Additionally, infected hepatocytes retain the capacity for CYP3A4 induction in response to treatment with phenobarbital, a uniquely sensitive indicator of hepatic differentiation status. Lentivectors may be used for both over-expression and knockdown analyses in primary hepatocytes, as demonstrated in this study by >200-fold CAR over-expression and knockdown of CAR to less than 40% of endogenous levels, with corresponding effects on CYP2B6 expression. In summary, lentiviral vectors provide a novel methodology by which primary human hepatocytes may be stably genetically manipulated, with minimal effects on the differentiated hepatic phenotype. These approaches offer considerable advantage over current methodologies, providing a valuable alternative for use in pharmacological and toxicological investigations involving primary human hepatocyte models and potentially for cell-based therapeutics to treat hepatic dysfunction in vivo.

Indexed as

Genetic VectorsPhenotypeTransduction, GeneticAdultAgedAryl Hydrocarbon HydroxylasesBase SequenceCell LineCells, CulturedConstitutive Androstane ReceptorCytochrome P-450 CYP2B6Cytochrome P-450 CYP3AFemaleGene Expression RegulationHepatocyte Nuclear Factor 4HepatocytesAryl Hydrocarbon HydroxylasesConstitutive Androstane ReceptorCYP2B6 protein, humanCYP3A4 protein, humanCytochrome P-450 CYP2B6Cytochrome P-450 CYP3AHepatocyte Nuclear Factor 4HNF4A protein, humanOxidoreductases, N-DemethylatingPregnane X ReceptorReceptors, Cytoplasmic and NuclearReceptors, SteroidRetinoid X Receptor alphaRNA, MessengerRNA, Small InterferingSerum AlbuminTranscription Factors

Identifiers

PMID18468591
PMCPMC2749468
OpenAlexW2095654167

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.