A1 Alkuperäisartikkeli tieteellisessä aikakauslehdessä
Glucagon-like peptide-1 receptor expression after myocardial infarction: Imaging study using [68Ga]NODAGA-exendin-4 positron emission tomography




Julkaisun tekijät: Mia Ståhle, Ville Kytö, Max Kiugel, Heidi Liljenbäck, Olli Metsälä, Meeri Käkelä, Xiang-Guo Li, Vesa Oikonen, Pekka Saukko, Pirjo Nuutila, Juhani Knuuti, Anne Roivainen, Antti Saraste
Kustantaja: Springer
Julkaisuvuosi: 2018
Journal: Journal of Nuclear Cardiology
Tietokannassa oleva lehden nimi: Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology
Lehden akronyymi: J Nucl Cardiol
ISSN: 1071-3581
eISSN: 1532-6551

Tiivistelmä

BACKGROUND:

Activation of glucagon-like peptide-1 receptor (GLP-1R) signaling protects against cardiac dysfunction and remodeling after myocardial infarction (MI). The aim of the study was to evaluate 68Ga-NODAGA-exendin-4 positron emission tomography (PET) for assessment of GLP-1R expression after MI in rats.

METHODS AND RESULTS:

Rats were studied at 3 days, 1 and 12 weeks after permanent coronary ligation or a sham-operation. Rats were injected with 68Ga-NODAGA-exendin-4 and scanned with PET and contrast-enhanced computed tomography (CT) followed by digital autoradiography and histology of left ventricle tissue sections. 68Ga-NODAGA-exendin-4 PET/CT showed focally increased tracer uptake in the infarcted regions peaking at 3 days and continuing at 1 week after MI. Pre-treatment with an unlabeled exendin-4 peptide significantly reduced 68Ga-NODAGA-exendin-4 uptake. By autoradiography, 68Ga-NODAGA-exendin-4 uptake was 8.6-fold higher in the infarcted region and slightly increased also in the remote, non-infarcted myocardium at 1 week and 12 weeks post-MI compared with sham. Uptake of 68Ga-NODAGA-exendin-4 correlated with the amount of CD68-positive macrophages in the infarcted area and alpha-smooth muscle actin staining in the remote myocardium.

CONCLUSIONS:

68Ga-NODAGA-exendin-4 PET detects up-regulation of cardiac GLP-1R expression during healing of MI in rats and may provide information on the activated repair mechanisms after ischemic myocardial injury.




Last updated on 2019-21-08 at 22:04