(11)C-Methionine PET Identifies Astroglia Involvement in Heart–Brain Inflammation Networking After Acute Myocardial Infarction
| Autor: | Frank M. Bengel, Yong Wang, Kai C. Wollert, Pablo Bascuñana, James T. Thackeray, Tobias Borchert, Annika Hess |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
Pathology
medicine.medical_specialty Integrin Inflammation 030204 cardiovascular system & hematology Cardiovascular 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine medicine Translocator protein Radiology Nuclear Medicine and imaging Myocardial infarction Methionine Microglia biology business.industry medicine.disease medicine.anatomical_structure chemistry biology.protein medicine.symptom Antibody business 030217 neurology & neurosurgery Immunostaining |
| Zdroj: | J Nucl Med |
| Popis: | Acute myocardial infarction (MI) triggers a local and systemic inflammatory response. We recently showed microglia involvement using translocator protein imaging. Here, we evaluated whether (11)C-methionine provides further insight into heart–brain inflammation networking. Methods: Male C57BL/6 mice underwent permanent coronary artery ligation followed by (11)C-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: (11)C-methionine uptake (percentage injected dose/cm(3)) 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 (11)C-methionine specifically identifies an astrocyte component, enabling further dissection of the heart–brain axis in post-MI inflammation. |
| Databáze: | OpenAIRE |
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