TY - JOUR T1 - <sup>11</sup>C-Methionine PET Identifies Astroglia Involvement in Heart–Brain Inflammation Networking After Acute Myocardial Infarction JF - Journal of Nuclear Medicine JO - J Nucl Med SP - 977 LP - 980 DO - 10.2967/jnumed.119.236885 VL - 61 IS - 7 AU - Pablo Bascuñana AU - Annika Hess AU - Tobias Borchert AU - Yong Wang AU - Kai C. Wollert AU - Frank M. Bengel AU - James T. Thackeray Y1 - 2020/07/01 UR - http://jnm.snmjournals.org/content/61/7/977.abstract N2 - 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 &lt; 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. ER -