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MRI monitoring of focal cerebral ischemia in peroxisome proliferator‐activated receptor (PPAR)‐deficient mice
Author(s) -
Pialat JeanBaptiste,
Cho TaeHee,
Beuf Olivier,
Joye Elisabeth,
Moucharaffie Samir,
Langlois JeanBaptiste,
Nemoz Chantal,
Janier Marc,
Berthezene Yves,
Nighoghossian Norbert,
Desvergne Béatrice,
Wiart Marlène
Publication year - 2007
Publication title -
nmr in biomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.278
H-Index - 114
eISSN - 1099-1492
pISSN - 0952-3480
DOI - 10.1002/nbm.1157
Subject(s) - neuroprotection , peroxisome proliferator activated receptor , receptor , lesion , ischemia , medicine , endocrinology , stroke (engine) , nuclear receptor , pathology , biology , biochemistry , physics , transcription factor , gene , thermodynamics
Peroxisome proliferator‐activated receptors (PPARs) are a potential target for neuroprotection in focal ischemic stroke. These nuclear receptors have major effects in lipid metabolism, but they are also involved in inflammatory processes. Three PPAR isotypes have been identified: α , β (or δ ) and γ . The development of PPAR transgenic mice offers a promising tool for prospective therapeutic studies. This study used MRI to assess the role of PPAR α and PPAR β in the development of stroke. Permanent middle cerebral artery occlusion induced focal ischemia in wild‐type, PPAR α ‐null mice and PPAR β ‐null mice. T 2 ‐weighted MRI was performed with a 7 T MRI scan on day 0, 1, 3, 7 and 14 to monitor lesion growth in the various genotypes. General Linear Model statistical analysis found a significant difference in lesion volume between wild‐type and PPAR‐null mice for both α and β isotypes. These data validate high‐resolution MRI for monitoring cerebral ischemic lesions, and confirm the neuroprotective role of PPAR α and PPAR β in the brain. Copyright © 2007 John Wiley & Sons, Ltd.