First Author | Hughes DM | Year | 2024 |
Journal | iScience | Volume | 27 |
Issue | 7 | Pages | 110244 |
PubMed ID | 39040070 | Mgi Jnum | J:352149 |
Mgi Id | MGI:7704765 | Doi | 10.1016/j.isci.2024.110244 |
Citation | Hughes DM, et al. (2024) The protective role of GATA6(+) pericardial macrophages in pericardial inflammation. iScience 27(7):110244 |
abstractText | Prior research has suggested that GATA6(+) pericardial macrophages may traffic to the myocardium to prevent interstitial fibrosis after myocardial infarction (MI), while subsequent literature claims that they do not. We demonstrate that GATA6(+) pericardial macrophages are critical for preventing IL-33 induced pericarditis and attenuate trafficking of inflammatory monocytes and granulocytes to the pericardial cavity after MI. However, absence of GATA6(+) macrophages did not affect myocardial inflammation due to MI or coxsackievirus-B3 induced myocarditis, or late-stage cardiac fibrosis and cardiac function post MI. GATA6(+) macrophages are significantly less transcriptionally active following stimulation in vitro compared to bone marrow-derived macrophages and do not induce upregulation of inflammatory markers in fibroblasts. This suggests that GATA6(+) pericardial macrophages attenuate inflammation through their interactions with surrounding cells. We therefore conclude that GATA6(+) pericardial macrophages are critical in modulating pericardial inflammation, but do not play a significant role in controlling myocardial inflammation or fibrosis. |