11C-Methionine PET Identifies Astroglia Involvement in Heart-Brain Inflammation Networking After Acute Myocardial Infarction
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PET Imaging of Neuroinflammation Using [11C]DPA-713 in a Mouse Model of Ischemic Stroke
Published on: June 14, 2018
Pablo Bascuñana1, Annika Hess1, Tobias Borchert1
1Department of Nuclear Medicine, Hannover Medical School, Hannover, Germany; and.
Abstract:
Acute myocardial infarction (MI) triggers a local and systemic inflammatory response. We recently showed microglia involvement using translocator protein imaging. Here, we evaluated whether 11C-methionine provides further insight into heart-brain inflammation networking. Methods: Male C57BL/6 mice underwent permanent coronary artery ligation followed by 11C-methionine PET at 3 and 7 d (n = 3). In subgroups, leukocyte homing was blocked by integrin antibodies (n = 5). The cellular substrate for PET signal was identified using brain section immunostaining. Results:11C-methionine uptake (percentage injected dose/cm3) peaked in the MI region on day 3 (5.9 ± 0.9 vs. 2.4 ± 0.5), decreasing to the control level by day 7 (4.3 ± 0.6). Brain uptake was proportional to cardiac uptake (r = 0.47, P < 0.05), peaking also on day 3 (2.9 ± 0.4 vs. 2.4 ± 0.3) and returning to baseline on day 7 (2.3 ± 0.4). Integrin blockade reduced uptake at every time point. Immunostaining on day 3 revealed colocalization of the l-type amino acid transporter, with glial fibrillary acidic protein-positive astrocytes but not CD68-positive microglia. Conclusion: PET imaging with 11C-methionine specifically identifies an astrocyte component, enabling further dissection of the heart-brain axis in post-MI inflammation.
Insights
Positron emission tomography (PET) with 11C-methionine reveals astrocyte involvement in the heart-brain axis after myocardial infarction (MI). This imaging technique helps dissect inflammation networks following heart attacks.
Area of Science:
- Neuroinflammation research
- Cardiovascular disease imaging
- Molecular imaging
Background:
- Acute myocardial infarction (MI) induces systemic inflammation, involving microglia.
- Previous studies utilized translocator protein imaging to assess microglial involvement.
- The role of astrocytes and heart-brain communication in post-MI inflammation requires further investigation.
Purpose of the Study:
- To evaluate 11C-methionine PET for insights into heart-brain inflammation networking post-MI.
- To identify the cellular basis of 11C-methionine uptake in the brain after cardiac injury.
- To explore the temporal dynamics of inflammation across the heart-brain axis.
Main Methods:
- Male C57BL/6 mice underwent permanent coronary artery ligation to induce MI.
- 11C-methionine PET imaging was performed at 3 and 7 days post-MI.
- Leukocyte homing was inhibited using integrin antibodies in subgroups.
- Brain sections were immunostained to identify cellular substrates of PET signals.
Main Results:
- 11C-methionine uptake peaked in the MI region and brain on day 3, decreasing by day 7.
- Cardiac and brain uptake of 11C-methionine showed a positive correlation.
- Integrin blockade reduced tracer uptake at all time points.
- Immunostaining identified astrocytes, not microglia, as the source of the PET signal via l-type amino acid transporter.
Conclusions:
- 11C-methionine PET imaging specifically visualizes astrocyte activation in the context of post-MI inflammation.
- This method allows for detailed analysis of the heart-brain axis communication.
- It provides a novel approach to understanding neuroinflammatory responses following myocardial infarction.
