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Gata6+ Pericardial Cavity Macrophages Relocate to the Injured Heart and Prevent Cardiac Fibrosis.
Immunity ( IF 25.5 ) Pub Date : 2019-07-16 , DOI: 10.1016/j.immuni.2019.06.010 Justin F Deniset 1 , Darrell Belke 2 , Woo-Yong Lee 1 , Selina K Jorch 1 , Carsten Deppermann 1 , Ali Fatehi Hassanabad 2 , Jeannine D Turnbull 2 , Guoqi Teng 2 , Isaiah Rozich 3 , Kelly Hudspeth 3 , Yuka Kanno 3 , Stephen R Brooks 4 , Anna-Katerina Hadjantonakis 5 , John J O'Shea 3 , Georg F Weber 6 , Paul W M Fedak 2 , Paul Kubes 7
Immunity ( IF 25.5 ) Pub Date : 2019-07-16 , DOI: 10.1016/j.immuni.2019.06.010 Justin F Deniset 1 , Darrell Belke 2 , Woo-Yong Lee 1 , Selina K Jorch 1 , Carsten Deppermann 1 , Ali Fatehi Hassanabad 2 , Jeannine D Turnbull 2 , Guoqi Teng 2 , Isaiah Rozich 3 , Kelly Hudspeth 3 , Yuka Kanno 3 , Stephen R Brooks 4 , Anna-Katerina Hadjantonakis 5 , John J O'Shea 3 , Georg F Weber 6 , Paul W M Fedak 2 , Paul Kubes 7
Affiliation
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Macrophages play an important role in structural cardiac remodeling and the transition to heart failure following myocardial infarction (MI). Previous research has focused on the impact of blood-derived monocytes on cardiac repair. Here we examined the contribution of resident cavity macrophages located in the pericardial space adjacent to the site of injury. We found that disruption of the pericardial cavity accelerated maladaptive post-MI cardiac remodeling. Gata6+ macrophages in mouse pericardial fluid contributed to the reparative immune response. Following experimental MI, these macrophages invaded the epicardium and lost Gata6 expression but continued to perform anti-fibrotic functions. Loss of this specialized macrophage population enhanced interstitial fibrosis after ischemic injury. Gata6+ macrophages were present in human pericardial fluid, supporting the notion that this reparative function is relevant in human disease. Our findings uncover an immune cardioprotective role for the pericardial tissue compartment and argue for the reevaluation of surgical procedures that remove the pericardium.
中文翻译：
Gata6 +心包腔巨噬细胞移至受伤的心脏并预防心脏纤维化。
巨噬细胞在结构性心脏重塑以及心肌梗死（MI）后向心力衰竭的转变中起着重要作用。先前的研究集中在血液来源的单核细胞对心脏修复的影响上。在这里，我们检查了位于心包空间中邻近损伤部位的常驻腔巨噬细胞的作用。我们发现，心包腔的破裂加速了心梗后适应不良的心脏重塑。小鼠心包液中的Gata6 +巨噬细胞有助于修复性免疫反应。实验性心肌梗死后，这些巨噬细胞侵入心外膜并失去Gata6表达，但继续发挥抗纤维化功能。缺血性损伤后，这种特殊的巨噬细胞种群的丧失会加剧间质纤维化。Gata6 +巨噬细胞存在于人心包液中，支持这种修复功能与人类疾病有关的观点。我们的发现揭示了心包组织区室的免疫心脏保护作用，并主张重新评估去除心包膜的手术程序。
更新日期：2019-07-17
中文翻译：
Gata6 +心包腔巨噬细胞移至受伤的心脏并预防心脏纤维化。
巨噬细胞在结构性心脏重塑以及心肌梗死（MI）后向心力衰竭的转变中起着重要作用。先前的研究集中在血液来源的单核细胞对心脏修复的影响上。在这里，我们检查了位于心包空间中邻近损伤部位的常驻腔巨噬细胞的作用。我们发现，心包腔的破裂加速了心梗后适应不良的心脏重塑。小鼠心包液中的Gata6 +巨噬细胞有助于修复性免疫反应。实验性心肌梗死后，这些巨噬细胞侵入心外膜并失去Gata6表达，但继续发挥抗纤维化功能。缺血性损伤后，这种特殊的巨噬细胞种群的丧失会加剧间质纤维化。Gata6 +巨噬细胞存在于人心包液中，支持这种修复功能与人类疾病有关的观点。我们的发现揭示了心包组织区室的免疫心脏保护作用，并主张重新评估去除心包膜的手术程序。
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