Dataset Information

A causal relation between bioluminescence and oxygen to quantify the cell niche.

ABSTRACT: Bioluminescence imaging assays have become a widely integrated technique to quantify effectiveness of cell-based therapies by monitoring fate and survival of transplanted cells. To date these assays are still largely qualitative and often erroneous due to the complexity and dynamics of local micro-environments (niches) in which the cells reside. Here, we report, using a combined experimental and computational approach, on oxygen that besides being a critical niche component responsible for cellular energy metabolism and cell-fate commitment, also serves a primary role in regulating bioluminescent light kinetics. We demonstrate the potential of an oxygen dependent Michaelis-Menten relation in quantifying intrinsic bioluminescence intensities by resolving cell-associated oxygen gradients from bioluminescent light that is emitted from three-dimensional (3D) cell-seeded hydrogels. Furthermore, the experimental and computational data indicate a strong causal relation of oxygen concentration with emitted bioluminescence intensities. Altogether our approach demonstrates the importance of oxygen to evolve towards quantitative bioluminescence and holds great potential for future microscale measurement of oxygen tension in an easily accessible manner.

SUBMITTER: Lambrechts D

PROVIDER: S-EPMC4026314 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

A causal relation between bioluminescence and oxygen to quantify the cell niche.

Lambrechts Dennis D Roeffaers Maarten M Goossens Karel K Hofkens Johan J Vande Velde Greetje G Van de Putte Tom T Schrooten Jan J Van Oosterwyck Hans H

PloS one 20140519 5

Bioluminescence imaging assays have become a widely integrated technique to quantify effectiveness of cell-based therapies by monitoring fate and survival of transplanted cells. To date these assays are still largely qualitative and often erroneous due to the complexity and dynamics of local micro-environments (niches) in which the cells reside. Here, we report, using a combined experimental and computational approach, on oxygen that besides being a critical niche component responsible for cellu ...[more]

PMID: 24840204

Similar Datasets

Project description:ObjectiveRecent epidemiological studies reported an association between maternal intake of acetaminophen (APAP) and attention deficit hyperactivity disorder (ADHD) in their children. However, none of these studies demonstrated causality. Our objective was to determine whether exposure to APAP during pregnancy result in hyperkinetic dysfunctions in offspring, using a murine model.Material and methodsPregnant CD1 mice (N = 8/group) were allocated to receive by gavage either APAP (150 mg/kg/day, equivalent to the FDA-approved maximum human clinical dose), or 0.5% carboxymethylcellulose (control group), starting on embryonic day 7 until delivery. Maternal serum APAP and alanine transaminase (ALT) concentrations were determined by ELISA and kinetic colorimetric assays, respectively. Open field locomotor activity (LMA) in the 30-day old mouse offspring was quantified using Photobeam Activity System. Mouse offspring were then sacrificed, whole brains processed for magnetic resonance imaging (MRI; 11.7 Tesla magnet) and for neuronal quantification using Nissl stain. The association between APAP exposure and LMA in mouse offspring was analyzed using a mixed effects Poisson regression model that accounted for mouse offspring weight, gender, random selection, and testing time and day. We corrected for multiple comparisons and considered P<0.008 as statistically significant.ResultsMaternal serum APAP concentration peaked 30 minutes after gavage, reaching the expected mean of 117 μg/ml. Serum ALT concentrations were not different between groups. There were no significant differences in vertical (rearing), horizontal, or total locomotor activity between the two rodent offspring groups at the P level fixed to adjust for multiple testing. In addition, no differences were found in volumes of 29 brain areas of interest on MRI or in neuronal quantifications between the two groups.ConclusionThis study refutes that hypothesis that prenatal exposure to APAP causes hyperkinetic dysfunction in mouse offspring. Due to lack of accurate assessment of ADHD in murine models, our results should be taken with caution when compared to the reported clinical data.

Project description:BackgroundShortening of gestation and intrauterine growth restriction (IUGR) are the two main determinants of birthweight. Low birthweight has been linked with prenatal arsenic exposure, but the causal relation between arsenic and birthweight is not well understood.ObjectivesWe applied a quantile causal mediation analysis approach to determine the association between prenatal arsenic exposure and birthweight in relation to shortening of gestation and IUGR, and whether the susceptibility of arsenic exposure varies by infant birth sizes.MethodsIn a longitudinal birth cohort in Bangladesh, we measured arsenic in drinking water (n=1182) collected at enrollment and maternal toenails (n=1104) collected ≤1-month postpartum using inductively coupled plasma mass spectrometry. Gestational age was determined using ultrasound at ≤16weeks' gestation. Demographic information was collected using a structured questionnaire.ResultsOf 1184 singleton livebirths, 16.4% (n=194) were low birthweight (<2500g), 21.9% (n=259) preterm (<37weeks' gestation), and 9.2% (n=109) both low birthweight and preterm. The median concentrations of arsenic in drinking water and maternal toenails were 2.2μg/L (range: below the level of detection [LOD]-1400) and 1.2μg/g (range: <LOD-46.6), respectively. Prenatal arsenic exposure was negatively associated with birthweight, where the magnitude of the association varied across birthweight percentiles. The effect of arsenic on birthweight mediated via shortening of gestation affected all infants irrespective of birth sizes (β range: 10th percentile=-19.7g [95% CI: -26.7, -13.3] to 90th percentile=-10.9g [95% CI: -18.5, -5.9] per natural log water arsenic increase), whereas the effect via pathways independent of gestational age affected only the smaller infants (β range: 10th percentile=-28.0g [95% CI: -43.8, -9.9] to 20th percentile=-14.9g [95% CI: -30.3, -1.7] per natural log water arsenic increase). Similar pattern was observed for maternal toenail arsenic.ConclusionsThe susceptibility of prenatal arsenic exposure varied by infant birth sizes, placing smaller infants at greater risk of lower birthweight by shortening of gestation and possibly growth restriction. It is important to mitigate prenatal arsenic exposure to improve perinatal outcomes in Bangladesh.

Dataset Information

A causal relation between bioluminescence and oxygen to quantify the cell niche.

Publications

A causal relation between bioluminescence and oxygen to quantify the cell niche.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets