RESEARCH ARTICLE


Spatial and Temporal MRI Profile of Ischemic Tissue after the Acute Stages of a Permanent Mouse Model of Stroke



Bogaert-Buchmann A 1, 2, Poittevin M 3, Po C 1, 2, Dupont D 1, 2, Sebrié C 1, 2, Tomita Y 3, TranDinh A3, Seylaz J3, Pinard E 3, Méric P 2, Kubis N 3, 4, Gillet B 1, 2, *
1 University Orsay Paris-sud, IR4M, UMR 8081, Bat 220, Orsay, F-91405, France
2 CNRS, Orsay, F-91405, France
3 INSERM U965, University. Paris 7, Angiogenèse et Recherche Translationelle, 2 rue Ambroise Paré, Paris, F-75475, France
4 AP-HP, Hôpital Lariboisière, Service de Physiologie, Université Paris Diderot, Sorbonne Paris Cité,, 2 rue Ambroise Paré, Paris, F-75475, France


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Creative Commons License
© Buchmann A et al; Licensee Bentham Open

open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

* Address correspondence to this author at the University Orsay Paris-sud, IR4M, UMR 8081, Bat 220, Orsay, F-91405, France; Tel: + 33 1 69 15 41 35; Fax: + 33 1 69 15 41 36; E-mail: brigitte.gillet@u-psud.fr


Abstract

Object:

To characterize the progression of injured tissue resulting from a permanent focal cerebral ischemia after the acute phase, Magnetic Resonance Imaging (MRI) monitoring was performed on adult male C57BL/6J mice in the subacute stages, and correlated to histological analyses.

Material and methods:

Lesions were induced by electrocoagulation of the middle cerebral artery. Serial MRI measurements and weighted-images (T2, T1, T2* and Diffusion Tensor Imaging) were performed on a 9.4T scanner. Histological data (Cresyl-Violet staining and laminin-, Iba1- and GFAP-immunostainings) were obtained 1 and 2 weeks after the stroke.

Results:

Two days after stroke, tissues assumed to correspond to the infarct core, were detected as a hyperintensity signal area in T2-weighted images. One week later, low-intensity signal areas appeared. Longitudinal MRI study showed that these areas remained present over the following week, and was mainly linked to a drop of the T2 relaxation time value in the corresponding tissues. Correlation with histological data and immuno-histochemistry showed that these areas corresponded to microglial cells.

Conclusion:

The present data provide, for the first time detailed MRI parameters of microglial cells dynamics, allowing its non-invasive monitoring during the chronic stages of a stroke. This could be particularly interesting in regards to emerging anti-inflammatory stroke therapies.

Keywords: Mouse, permanent cerebral ischemia, stroke, microglia, NMR Imagingz.