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Cardiac macrophages in wound healing following myocardial infarction: from experiment to clinic A. Gombozhapova, Y. V. Rogovskaya, M. Rebenkova [et al.]

Contributor(s): Gombozhapova, Aleksandra | Rogovskaya, Yuliya V | Rebenkova, Mariya | Kzhyshkowska, Julia G | Ryabov, Vyacheslav VMaterial type: ArticleArticleContent type: Текст Media type: электронный Subject(s): макрофаги | регенерация миокарда | инфаркт миокардаGenre/Form: статьи в журналах Online resources: Click here to access online In: European heart journal: Acute cardiovascular care Vol. 7, suppl. № 1. P. 178-179Abstract: Introduction: Macrophages are key innate immune cells that play a significant role in transition from inflammatory to regenerative phase during wound healing following myocardial infarction (MI). Despite the progress of experimental studies devoted to the innate immune response following MI, there is no significant advancement in clinical studies. Purpose: The purpose of the research was to translate experimental knowledge regarding macrophage subsets and their biomarkers in post infarction left ventricular remodeling and myocardial regeneration into results observed in clinical settings. We suggested protocol based on usage of macrophage biomarkers to study cellular basis of cardiac remodeling and healing in patients with MI. Methods: The study included 41 patients with fatal MI type 1. All patients were divided into 4 groups depending on the timeline of MI histopathology. In addition to routine histopathological analysis macrophages infiltration was assessed by immunohistochemistry. We used CD68 as a marker for the cells of the macrophage lineage, while CD163 and stabilin-1 were considered as M2-like macrophage biomarkers. Nine patients who died from non-cardiovascular causes comprised the control group. Results: The figure (Figure 1) demonstrates results of immunohistochemical analysis. In the control group the number of CD68+ and CD163+ macrophages was lower than in the infarct, peri-infarct and non-infarct areas during all phases of MI (p < 0.001). Simultaneously the quantity of stabilin-1+ cells in the control group was higher in all the areas during inflammatory phase of MI (p=0.01). We noticed that numbers of CD68+, CD163+ and stabilin-1+ macrophages depended on MI phase. The number of CD68+ cells correlated with the day of MI: strong positive correlation was found in the infarct area (R=0.67, p=0.001) and moderate positive correlation was noticed in the peri-infarct area (R=0.55, p < 0.001). There was similar relationship for CD163+ (infarct area: R=0.61, p=0.001; peri-infarct area: R=0.66, p < 0.001) and stabilin-1+ cells (infarct area: R=0.6, p < 0.001; peri-infarct area: R=0.42, p=0.007). Conclusions: Our study translated experimental knowledge regarding macrophage subpopulations in post-infarction myocardial regeneration into clinical. We observed cardiac macrophage response following MI reminded a murine model. Our data indicate following: (1) dichotomous M1-M2 model is not sufficient to completely describe functions of macrophage subsets; (2) characterization of macrophage phenotypes by multiple biomarkers is promising; (3) stabilin-1 could be used as macrophage biomarker in cardiac wound healing in patients with MI. Our study supported diagnostic prospects for implementation of macrophage phenotyping in clinic. Identifying effective biomarkers of different macrophage subsets in patients with MI might become the basis of the method to predict adverse cardiac remodeling and the first step to develop myocardial regeneration target therapy.
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Introduction: Macrophages are key innate immune cells that play a significant role in transition from inflammatory to regenerative phase during wound healing following myocardial infarction (MI). Despite the progress of experimental studies devoted to the innate immune response following MI, there is no significant advancement in clinical studies. Purpose: The purpose of the research was to translate experimental knowledge regarding macrophage subsets and their biomarkers in post infarction left ventricular remodeling and myocardial regeneration into results observed in clinical settings. We suggested protocol based on usage of macrophage biomarkers to study cellular basis of cardiac remodeling and healing in patients with MI. Methods: The study included 41 patients with fatal MI type 1. All patients were divided into 4 groups depending on the timeline of MI histopathology. In addition to routine histopathological analysis macrophages infiltration was assessed by immunohistochemistry. We used CD68 as a marker for the cells of the macrophage lineage, while CD163 and stabilin-1 were considered as M2-like macrophage biomarkers. Nine patients who died from non-cardiovascular causes comprised the control group. Results: The figure (Figure 1) demonstrates results of immunohistochemical analysis. In the control group the number of CD68+ and CD163+ macrophages was lower than in the infarct, peri-infarct and non-infarct areas during all phases of MI (p < 0.001). Simultaneously the quantity of stabilin-1+ cells in the control group was higher in all the areas during inflammatory phase of MI (p=0.01). We noticed that numbers of CD68+, CD163+ and stabilin-1+ macrophages depended on MI phase. The number of CD68+ cells correlated with the day of MI: strong positive correlation was found in the infarct area (R=0.67, p=0.001) and moderate positive correlation was noticed in the peri-infarct area (R=0.55, p < 0.001). There was similar relationship for CD163+ (infarct area: R=0.61, p=0.001; peri-infarct area: R=0.66, p < 0.001) and stabilin-1+ cells (infarct area: R=0.6, p < 0.001; peri-infarct area: R=0.42, p=0.007). Conclusions: Our study translated experimental knowledge regarding macrophage subpopulations in post-infarction myocardial regeneration into clinical. We observed cardiac macrophage response following MI reminded a murine model. Our data indicate following: (1) dichotomous M1-M2 model is not sufficient to completely describe functions of macrophage subsets; (2) characterization of macrophage phenotypes by multiple biomarkers is promising; (3) stabilin-1 could be used as macrophage biomarker in cardiac wound healing in patients with MI. Our study supported diagnostic prospects for implementation of macrophage phenotyping in clinic. Identifying effective biomarkers of different macrophage subsets in patients with MI might become the basis of the method to predict adverse cardiac remodeling and the first step to develop myocardial regeneration target therapy.

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