PuSH - Publication Server of Helmholtz Zentrum München: Genetically controlled uptake of ferritin as an MRI contrast agent.

Information

Clues to quality of journals

Open Access Policy of Helmholtz Association 2016

CC Licencences

Publication Metrics

Navigation

Home

Deutsch

EVA: Electronic Publishing

New EVA Application

Research

Advanced Search

Browse by ...

... HMGU-Authors/Consortia

... Organizational Structure

... Journal

... Publication Type

... Research Data

... Arbeitsgruppen

... Publication Year

Publication overview

Statistics

Statistics (last 5 years)

OA Publications

Publish

Submit Publication

Import publication from...

...EVA

Report missing publication

Highlights

Support & Contact

Contact persons

Help

Data protection

Helmholtz Open Science

JANE Journal Estimator

SHERPA/RoMEO

DOAJ

Export:

Text

Endnote (RIS) BIB

BibTeX

Massner, C. ; Pariani, G. ; Rolbieski, H. ; Sigmund, F. ; Westmeyer, G.G.

Genetically controlled uptake of ferritin as an MRI contrast agent.

Am. J. Hematol. 91, E119 (2016)

Open Access Green as soon as Postprint is submitted to ZB.

Abstract
Metrics
Extra information

Throughout recent years our understanding of iron trafficking and storage on a cellular level has been growing immensely. This knowledge can be utilized for developing of genetically controlled MRI contrast agents for applications in noninvasive preclinical gene reporter imaging of entire organisms. We measured the T2 relaxation rates of HEK293T cells loaded with ferritin during overexpression of transferrin receptor 1 (TfR1) and yellow fluorescent protein (YFP) as a control. The cell viability was determined by trypan blue staining and cell counting. The intracellular iron content was calculated based on a ferrozine assay1 and cell count. The elevated uptake of horse spleen ferritin (HSFt) in HEK293T overexpressing TfR1 resulted in 60% increased T2 relaxation rate after one or two days expression of the respective proteins without observable toxic effects. Our results show that genetic control over ferritin uptake through the overexpression of TfR1 results in elevated MRI contrast and cellular iron loading. As reported, this probably occurs via ferritin binding on the cell surface receptor and subsequent internalization. Since ferrihydrite can be exchanged by more magnetizable iron pecies in the ferritin cavity3 and ferritin can cross the blood brain barrier4, this system has the potential to outperform superparamagnetic iron-oxide (SPIO) based imaging in brain research with respect to delivery and cell specific addressability.