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MAIR-II deficiency ameliorates cardiac dysfunction post-myocardial infarction by suppressing TLR9-mediated pro-inflammatory macrophage activation

米林, 沙織 筑波大学 DOI:10.15068/0002000725

2021.07.28

概要

Purpose: Myocardial infarction (MI) is one of the highest causes of mortality as a result of ischemic cardiovascular disease. In the post-MI response, macrophages infiltrate the site of injury leading to inflammation, adverse cardiac remodeling, and heart failure. However, the underlying mechanisms in regulating macrophage activation in the post-MI inflammatory response have not been fully elucidated. Myeloid-associated immunoglobulin-like receptor II (MAIR-II) is a cell surface receptor on macrophages and a subset of B cells. Previous studies have shown that MAIR-II mediates pro-inflammatory cytokine production in macrophages. However, its role in MI is unknown. In this study, the novel role and mechanism of MAIR-II in inflammation and macrophages in MI was identified.

Materials and Methods: To address MAIR-II’s role in MI in vivo, an MI mouse model of permanent left coronary artery ligation was utilized. To determine MAIR-II’s expression levels and time course in infarcted C57BL/6J (WT) hearts, quantitative-polymerase chain reaction (q-PCR) was used to evaluate MAIR-II’s gene expression and flow cytometry was used to assess MAIR-II’s expression on myeloid cells post-MI. To determine the effects of MAIR-II in the post-MI response, WT and MAIR-II deficient (Cd300c2-/-) mice were utilized. Post-MI survival was assessed by conducting a Kaplan Meier survival curve analysis, cardiac remodeling was evaluated by echocardiography analysis, and effects on infarct size were determined by Masson trichrome staining. For further investigation, pro-inflammatory and pro-fibrotic cytokine expression were measured in infarcted heart tissue by q-PCR. Moreover, the accumulation of macrophages, anti-inflammatory macrophages, and pro-inflammatory macrophages was observed in infarcted hearts by flow cytometry. Finally, to elucidate MAIR-II’s molecular mechanism in vitro, pro-inflammatory and anti-inflammatory cytokine expressions were measured from Cd300c2-/- and WT bone marrow-derived macrophages (BMDMs) stimulated by a toll-like receptor (TLR)9 ligand ODN1668 or a simultaneous stimulation of ODN1668 and a TLR9 antagonist ODN2088.

Results: MAIR-II positive myeloid cells were abundant from post-MI days 3 to 5 in infarcted hearts of WT mice. Furthermore, Cd300c2-/- mice had a higher post-MI survival rate than WT mice (p=0.043). In echocardiography, Cd300c2-/- mice had thicker left ventricle posterior walls and higher ejection fractions compared to WT mice post-MI. After further investigation, Cd300c2-/- hearts had less pro-inflammatory IL-1β and less F4/80+CD206low pro-inflammatory macrophages in infarcted hearts compared to WT. Upon stimulation with a TLR9 ligand, Cd300c2-/- BMDMs produced less inflammatory cytokines such as IL-1β and IL-6.

Discussion: MAIR-II may increase pro-inflammatory macrophage infiltration and subsequent pro-inflammatory cytokine production via TLR9, leading to exacerbated post-MI inflammation. Therefore, modified macrophage responses by MAIR-II in post-MI inflammation can lead to harmful effects including enlarged infarct size and higher mortality. In the current study, the length of infarct segments was shorter in Cd300c2-/- mice compared to WT. After further investigation, there were more surviving cardiomyocytes in the infarcted area of Cd300c2-/- than in that of WT. These findings imply that the infarcted area with few remaining cardiomyocytes may be vulnerable to wall stress and thus become more stretched. Moreover, necrotic cells or damaged living cells release damage-associated molecular patterns (DAMPs), which are recognized by pattern-recognition receptors such as TLRs. In MI, necrotic cardiac cells release mitochondrial DNA (mtDNA) and acts as a DAMP, activating TLR9-dependent NF-κB inflammation. Thus, this study suggests that macrophage activation via MAIR-II and TLR9 can cause excessive post-MI inflammation thus increasing cardiac necrosis and enlarges infarct size. Future clinical applications of MAIR-II can be considered during the acute inflammatory phase of post-MI to ensure favorable late phase effects. This study suggests that MAIR-II promotes inflammation and thereby fibrosis during the early stage after MI, leading to poor prognosis during the late stage. Furthermore, elevated levels of MAIR-II in myocardial tissue can be an indicator of post-MI severity. Thus, reducing MAIR-II levels in the early stages of post-MI may prevent the worsening of adverse cardiac events over time.

Conclusion: MAIR-II may enhance TLR9-mediated pro-inflammatory macrophage activation in MI, leading to adverse cardiac remodeling and poor prognosis.

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