Evidence map›Paper›PMID 26365578›Full record

ArticleThe Journal of nutritional biochemistry2015

Amino acid starvation induced by protease inhibition produces differential alterations in redox status and the thiol proteome in organogenesis-stage rat embryos and visceral yolk sacs.

Craig Harris, Joseph L Jilek, Karilyn E Sant, Jan Pohl, Matthew Reed, Jason M Hansen

Open access · greenAbstract read
In one paragraph

Article in The Journal of nutritional biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

4 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. 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

6 authors at 3 institutions in 1 country.

Craig HarrisToxicology Program, Department of Environmental Health Sciences, University of Michigan, Ann Arbor, MI 48109-2029. Electronic address: charris@umich.edu.
Joseph L JilekToxicology Program, Department of Environmental Health Sciences, University of Michigan, Ann Arbor, MI 48109-2029.
Karilyn E SantToxicology Program, Department of Environmental Health Sciences, University of Michigan, Ann Arbor, MI 48109-2029.
Jan PohlBiotechnology Core Facility Branch, Centers for Disease Control/DSR, Atlanta, GA 30333.
Matthew ReedBiotechnology Core Facility Branch, Centers for Disease Control/DSR, Atlanta, GA 30333.
Jason M HansenDepartment of Physiology and Developmental Biology, Brigham Young University, Provo, UT, 84602.
University of Michigan–Ann Arbor · USCenters for Disease Control and Prevention · USBrigham Young University · US

Funding

Strategic Vision & Impact on Environmental HealthP30ES017885 · NIEHS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Dana Dolinoy · 2011 to 2026
$21.3M
ENVIRONMENTAL TOXICOLOGY PRE/POST DOCTORAL RES.TRAININGT32ES007062 · NIEHS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Justin Adam Colacino · 1985 to 2026
$10.5M
NIEHS NIH HHS P30 ES017885NIEHS NIH HHS T32 ES007062
6 · The paper itself

Abstract

The process of embryonic nutrition in rodent conceptuses during organogenesis has been shown to involve a dominant histiotrophic mechanism where essential developmental substrates and micronutrients are supplied as whole maternal proteins or cargoes associated with proteins. The histiotrophic nutrition pathways (HNP) responsible for uptake and initial processing of proteins across maternal-conceptal interfaces involve uptake via receptor mediated endocytosis and protein degradation via lysosomal proteolysis. Chemical inhibition of either process can lead to growth deficits and malformation in the embryo (EMB), but selective inhibition of either HNP component will elicit a different subset of developmental perturbations. In vitro, whole embryo culture exposure of GD10 or GD11 rat conceptuses to the natural protease inhibitor, leupeptin, leads to significant reductions in all measured embryonic growth parameters as well as a myriad of other effects. Leupeptin doses of 10 μM or 20 μM over a 26-h period (GD10-GD11) and 50 μM over a 3 h pulse period produced significant decreases in the clearance of FITC-albumin from culture media. The near complete loss of acid soluble fluorescence and increased total visceral yolk sac (VYS) protein content confirmed the selective inhibition of proteolysis. Inhibition of lysosomal proteolysis thus deprives the developing EMB of essential nutrient amino acids producing conditions akin to amino acid starvation, but may also cause direct effects on pathways critical for normal growth and differentiation. Following leupeptin exposure for 26 or 6 h, total glutathione (GSH) concentrations dropped significantly in the VYS, but only slightly in yolk sac (YSF) and amniotic (AF) fluids. Cys concentrations increased in VYS and EMB, but dropped in YSF and AF fluids. Redox potentials (Eh) for the glutathione disulfide (GSSG)/glutathione (GSH) redox couple trended significantly toward the positive, confirming the net oxidation of conceptual tissues following leupeptin treatment. Analysis of the thiol proteome showed few alterations to specific pathways mapped to the Kyoto Encyclopedia of Genes and Genomes Pathway database, but did reveal significant increases in concentrations of proteins associated with glycolysis/gluconeogenesis in the VYS and decreased concentrations proteins associated with ribosome biogenesis and function in the EMB. A subset of proteins elevated by >2-23-fold in the VYS were identified as serum (blood) proteins and represent the maternal-side proteins captured by the VYS and which are not degraded in the lysosomes as a result of leupeptin's inhibitory action. The observed constellation of proteins decreased in the EMB by leupeptin represent proteins from several adaptive pathways that are commonly altered in responses to amino acid starvation. These studies show clear differential responses to protease inhibition in VYS and EMB during organogenesis and suggest the possibility for additional roles of redox regulation, cellular adaptations and metabolic insufficiency caused by protease inhibition.

Indexed as

Gene Expression Regulation, EnzymologicAmino AcidsAnimalsCulture MediaDose-Response Relationship, DrugGlutathioneLeupeptinsLysosomesOrganogenesisOxidation-ReductionProtease InhibitorsProteolysisProteomeRatsRats, Sprague-DawleyReactive Oxygen SpeciesAmino AcidsCulture MediaGlutathioneleupeptinLeupeptinsProtease InhibitorsProteomeReactive Oxygen SpeciesSulfhydryl CompoundsAmino acid starvationEmbryoLeupeptinProtease inhibitionRedox potentialThiol proteomeVisceral yolk sac

Identifiers

PMID26365578
PMCPMC4679479
OpenAlexW1202260141

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.