11C-Methionine PET Identifies Astroglia Involvement in Heart–Brain Inflammation Networking After Acute Myocardial Infarction
Immunostaining
CD68
DOI:
10.2967/jnumed.119.236885
Publication Date:
2019-12-05T23:45:14Z
AUTHORS (7)
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 <sup>11</sup>C-methionine provides further insight into heart–brain inflammation networking. <b>Methods:</b> Male C57BL/6 mice underwent permanent coronary artery ligation followed by PET at 3 7 d (<i>n</i> = 3). In subgroups, leukocyte homing was blocked integrin antibodies 5). The cellular substrate for signal identified brain section immunostaining. <b>Results:</b><sup>11</sup>C-methionine uptake (percentage injected dose/cm<sup>3</sup>) peaked in the MI region on day (5.9 ± 0.9 vs. 2.4 0.5), decreasing to control level (4.3 0.6). Brain proportional cardiac (<i>r</i> 0.47, <i>P</i> < 0.05), peaking also (2.9 0.4 0.3) returning baseline (2.3 0.4). Integrin blockade reduced every time point. Immunostaining revealed colocalization of l-type amino acid transporter, with glial fibrillary acidic protein–positive astrocytes but not CD68-positive microglia. <b>Conclusion:</b> imaging specifically identifies an astrocyte component, enabling dissection axis post-MI inflammation.
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