scholarly journals Macrophage Polarization in Cardiac Tissue Repair Following Myocardial Infarction

2021 ◽  
Vol 22 (5) ◽  
pp. 2715
Author(s):  
Yevgeniy Kim ◽  
Sanzhar Nurakhayev ◽  
Ayan Nurkesh ◽  
Zharylkasyn Zharkinbekov ◽  
Arman Saparov
Keyword(s):  
Myocardial Infarction ◽  
Cardiovascular Disease ◽  
Cardiac Tissue ◽  
Macrophage Polarization ◽  
Scar Tissue ◽  
M1 Macrophages ◽  
Mortality And Morbidity ◽  
Phenotypic Profile ◽  
Detrimental Impact ◽  
Alternatively Activated

Cardiovascular disease is the leading cause of mortality and morbidity around the globe, creating a substantial socio-economic burden as a result. Myocardial infarction is a significant contributor to the detrimental impact of cardiovascular disease. The death of cardiomyocytes following myocardial infarction causes an immune response which leads to further destruction of tissue, and subsequently, results in the formation of non-contractile scar tissue. Macrophages have been recognized as important regulators and participants of inflammation and fibrosis following myocardial infarction. Macrophages are generally classified into two distinct groups, namely, classically activated, or M1 macrophages, and alternatively activated, or M2 macrophages. The phenotypic profile of cardiac macrophages, however, is much more diverse and should not be reduced to these two subsets. In this review, we describe the phenotypes and functions of macrophages which are present in the healthy, as well as the infarcted heart, and analyze them with respect to M1 and M2 polarization states. Furthermore, we discuss therapeutic strategies which utilize macrophage polarization towards an anti-inflammatory or reparative phenotype for the treatment of myocardial infarction.

scholarly journals Wheat germ agglutinin staining as a suitable method for detection and quantification of fibrosis in cardiac tissue after myocardial infarction

2014 ◽  
Author(s):  
B. Emde ◽  
A. Heinen ◽  
A. Gödecke ◽  
K. Bottermann
Keyword(s):  
Myocardial Infarction ◽  
Wheat Germ Agglutinin ◽  
Wheat Germ ◽  
Cardiac Fibrosis ◽  
Cardiac Tissue ◽  
Scar Tissue ◽  
Color Contrast ◽  
Tissue Sections ◽  
Fibrotic Tissue ◽  
Frozen Tissue

The quantification of fibrotic tissue is an important task in the analysis of cardiac remodeling. The use of established fibrosis staining techniques is limited on frozen cardiac tissue sections due to a reduced color contrast compared to paraffin embedded sections. We therefore used FITC-labeled wheat germ agglutinin (WGA), which marks fibrotic tissue in comparable quality as the established picrosirius red (SR) staining, for the staining of post myocardial infarction scar tissue. The fibrosis amount was quantified in a histogram-based approach using the non-commercial image processing program ImageJ. Our results clearly demonstrate that WGA-FITC is a suitable marker for cardiac fibrosis in frozen tissue sections. In combination with the histogram-based analysis, this new quantification approach is i) easy and fast to perform; ii) suitable for raw frozen tissue sections; and iii) allows the use of additional antibodies in co-immunostaining. 

scholarly journals Inflammation and macrophage polarization in cutaneous melanoma: Histopathological and immunohistochemical study

2016 ◽  
Vol 29 (4) ◽  
pp. 715-719 ◽  
Author(s):  
Elisabetta Scali ◽  
Chiara Mignogna ◽  
Anna Di Vito ◽  
Ivan Presta ◽  
Caterina Camastra ◽  
...  
Keyword(s):  
Cutaneous Melanoma ◽  
Dynamic Balance ◽  
Macrophage Polarization ◽  
Polarization State ◽  
Lymphocytic Infiltrate ◽  
Histopathological Analysis ◽  
Superficial Spreading ◽  
M1 Macrophages ◽  
Melanoma Prognosis ◽  
Alternatively Activated

Tumor-associated macrophages (TAMs) are considered to affect tumor growth and progression. Macrophages can be classified into two states of polarized activation, namely classically activated M1 macrophages and alternatively activated M2 macrophages. The dynamic balance between TAMs and tumor cells has an important impact on tumor homeostasis and progression. The aim of this study was to characterize the phenotype of TAMs present in different subtypes of superficial spreading cutaneous melanoma and their relationship with the lymphocytic infiltrate in order to identify new histopathological tools for melanoma prognosis and suitable targets for melanoma therapy. We selected four groups of patients with malignant melanoma in order to analyze the profile of polarized macrophage activation using immunohistochemical methods. Histopathological analysis showed that the macrophage polarization state appears to be more related to the lymphocytic infiltrate than to the thickness of the lesions. Further studies are necessary to increase understanding of the immunopathological dynamic of melanoma that may be modulated by future targeted immunotherapies.

scholarly journals Anti-Inflammatory Effect of Curcumin on the Mouse Model of Myocardial Infarction through Regulating Macrophage Polarization

2021 ◽  
Vol 2021 ◽  
pp. 1-19
Author(s):  
Shaoxi Yan ◽  
Mo Zhou ◽  
Xiaoyun Zheng ◽  
Yuanyuan Xing ◽  
Juan Dong ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Ventricular Remodeling ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
M1 Macrophages ◽  
Macrophage Marker ◽  
M1 Macrophage ◽  
Anti Inflammatory

Inflammation causes tissue damage and promotes ventricular remodeling after myocardial infarction (MI), and the infiltration and polarization of macrophages play an important role in regulating inflammation post-MI. Here, we investigated the anti-inflammatory function of curcumin after MI and studied its relationship with macrophage polarization. In vivo, curcumin not only attenuated ventricular remodeling 3 months after MI but also suppressed inflammation during the first 7 days post-MI. Importantly, the results of qPCR and immunochemistry showed that curcumin decreased M1 (iNOS, CCL2, and CD86) but increased M2 macrophage (Arg1, CD163, and CD206) marker expression in the myocardium of MI mice during the first 7 days post-MI. And flow cytometry analysis indicated that curcumin suppressed M1 (CD45+Gr-1-CD11b+iNOS+ cells) but enhanced M2 macrophage (CD45+Gr-1-CD11b+Arg+ cells) expansion in the myocardium of MI mice during the first 7 days post-MI. In vitro, curcumin decreased LPS/IFNγ-elevated M1 macrophage marker (iNOS and CD86) expression and the proportion of M1 macrophages (iNOS+F4/80+ cells) but increased LPS/IFNγ-suppressed M2 macrophage marker (Arg1 and CD206) expression and the proportion of M2 macrophages (Arg1+F4/80+ cells). In addition, curcumin modulates M1/M2 macrophage polarization partly via AMPK. In conclusion, curcumin suppressed the MI-induced inflammation by modulating macrophage polarization partly via the AMPK pathway.

scholarly journals Epicardial therapy with atrial appendage micrografts salvages myocardium after infarction

2019 ◽  
Author(s):  
Xie Yanbo ◽  
Milla Lampinen ◽  
Juuso Takala ◽  
Vilbert Sikorski ◽  
Rabah Soliymani ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Extracellular Matrix ◽  
Cardiac Tissue ◽  
Artery Bypass ◽  
Cardiac Regeneration ◽  
Atrial Appendage ◽  
Mortality And Morbidity ◽  
The Matrix ◽  
Clinical Benefits ◽  
Matrix Patch

AbstractIschemic heart disease remains the leading cause of mortality and morbidity worldwide despite improved possibilities in medical care. Alongside interventional therapies, such as coronary artery bypass grafting, adjuvant tissue-engineered and cell-based treatments can provide regenerative improvement. Unfortunately, most of these advanced approaches require multiple lengthy and costly preparation stages without delivering significant clinical benefits.We evaluated the effect of epicardially delivered minute pieces of atrial appendage tissue material, defined as atrial appendage micrografts (AAMs), in mouse myocardial infarction model. An extracellular matrix patch was used to cover and fix the AAMs onto the surface of the infarcted heart. The matrix-covered AAMs salvaged the heart from infarction-induced loss of functional myocardium and attenuated scarring. Site-selective proteomics of injured ischemic and uninjured distal myocardium from AAM-treated and untreated tissue sections revealed an increased expression of several cardiac regeneration-associated proteins (i.e. periostin, transglutaminases and glutathione peroxidases) as well as activation of pathways responsible for angio- and cardiogenesis in relation to AAMs therapy.Epicardial delivery of AAMs encased in an extracellular matrix patch scaffold salvages functional cardiac tissue from ischemic injury and restricts fibrosis after myocardial infarction. Our results support the use of AAMs as tissue-based therapy adjuvants for salvaging the ischemic myocardium.

scholarly journals Biomimetic nanovesicle design for cardiac tissue repair

Nanomedicine ◽  
2020 ◽  
Vol 15 (19) ◽  
pp. 1873-1896
Author(s):  
Sruti Bheri ◽  
Jessica R Hoffman ◽  
Hyun-Ji Park ◽  
Michael E Davis
Keyword(s):  
Cardiovascular Disease ◽  
Tissue Repair ◽  
Cardiac Tissue ◽  
Cardiac Repair ◽  
Parent Cell ◽  
Target Tissue ◽  
High Uptake ◽  
Mortality And Morbidity ◽  
Potential Value ◽  
Future Potential

Cardiovascular disease is a major cause of mortality and morbidity worldwide. Exosome therapies are promising for cardiac repair. Exosomes transfer cargo between cells, have high uptake by native cells and are ideal natural carriers for proteins and nucleic acids. Despite their proreparative potential, exosome production is dependent on parent cell state with typically low yields and cargo variability. Therefore, there is potential value in engineering exosomes to maximize their benefits by delivering customized, potent cargo for cardiovascular disease. Here, we outline several methods of exosome engineering focusing on three important aspects: optimizing cargo, homing to target tissue and minimizing clearance. Finally, we put these methods in context of the cardiac field and discuss the future potential of vesicle design.

scholarly journals CDC-derived extracellular vesicles reprogram inflammatory macrophages to an arginase 1-dependent proangiogenic phenotype

2020 ◽  
Vol 318 (6) ◽  
pp. H1447-H1460 ◽  
Author(s):  
Kyle I. Mentkowski ◽  
Asma Mursleen ◽  
Jonathan D. Snitzer ◽  
Lindsey M. Euscher ◽  
Jennifer K. Lang
Keyword(s):  
Myocardial Infarction ◽  
Extracellular Vesicles ◽  
Macrophage Polarization ◽  
Extracellular Vesicle ◽  
Primary Target ◽  
Relevant Model ◽  
M1 Macrophages ◽  
Arginase 1 ◽  
Inflammatory Macrophages ◽  
Insight Into

We hypothesized that in the window of therapeutic extracellular vesicle (EV) administration, inflammatory M1 macrophages are likely the primary target of cardiosphere-derived cell (CDC)-derived EVs. The effect of CDC-EVs on this population, however, is currently unknown. In this study, we demonstrate that CDC-derived EVs polarize M1 macrophages to a proangiogenic phenotype dependent on arginase 1 upregulation. These results provide insight into an immunomodulatory mechanism of CDC-EVs in a more physiologically relevant model of post-myocardial infarction (post-MI) macrophage polarization.

Surface-modified polymers for cardiac tissue engineering

2017 ◽  
Vol 5 (10) ◽  
pp. 1976-1987 ◽  
Author(s):  
Ambigapathi Moorthi ◽  
Yu-Chang Tyan ◽  
Tze-Wen Chung
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Cardiovascular Disease ◽  
Tissue Engineering ◽  
Causes Of Death ◽  
Cardiac Tissue ◽  
Cardiac Tissue Engineering ◽  
Modified Polymers ◽  
Surface Modified

Cardiovascular disease (CVD), leading to myocardial infarction and heart failure, is one of the major causes of death worldwide.

scholarly journals Management and Outcomes of ST-segment Elevation Myocardial Infarction During Coronavirus 2019 Pandemic in a Center with 24/7 Primary Angioplasty Capability: Should We Change Our Practice During Outbreak?

2020 ◽  
Author(s):  
Mojtaba Salarifar ◽  
Mojgan Ghavami ◽  
Hamidreza Poorhosseini ◽  
Farzad Masoudkabir ◽  
Yaser Jenab ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Tissue ◽  
Tissue Injury ◽  
Coronary Intervention ◽  
Primary Angioplasty ◽  
Ct Imaging ◽  
Cardiac Events ◽  
Mortality And Morbidity ◽  
St Segment Elevation ◽  
The Difference

AbstractBackgroundST-Elevation Myocardial Infarction (STEMI) is associated with high mortality and morbidity. In order to minimize cardiac tissue injury, primary per-cutaneous coronary intervention (PPCI) as treatment of choice should be performed as soon as possible. Coronavirus Disease 2019 (COVID-19) as an ongoing major global concern affects the other parts of health care system. Applying preventive strategies during this outbreak is necessary. However, critical times in STEMI management and outcomes may be influenced by infection control protocols implementation. The aim of this study is to investigate the differences in time intervals related to STEMI care and 15-day major adverse cardiac events (MACE) during this outbreak compared with the same period in last year and to determine whether the STEMI protocol should be changed to thrombolytic therapy during COVID-19 outbreak or not.MethodsThe patients with STEMI who underwent PPCI in Tehran Heart Center were included. Chest Computed tomography (CT) imaging and real time Reverse Transcription Polymerase Chain Reaction (rRT-PCR) were only performed for COVID-19 suspected patients. Seventy-seven patients from 29th February to 29th March 2020 were compared with 62 patients from 1st to 30th March 2019.ResultsCOVID-19 infection was confirmed by rRT-PCR in 5 cases. CT imaging in 4 out of 5 patients was in favor of COVID-19. The median of door-to-device time was reduced 13 minutes during this outbreak (p: 0.007). In-hospital mortality before and during outbreak was 3.22% and 5.19%, respectively (p: 0.57). Confirmed infection with COVID-19 was only reported in one of expired cases. The difference in 15-day MACE between two time periods was not statistically significant.Discussion/ConclusionGiven that 15-day outcome in acute STEMI patients is not affected by COVID-19 outbreak, we did not find it reasonable to change our protocol. However, further studies are needed to determine a standard protocol for emergency management.

scholarly journals Defects in Macrophage Reprogramming in Cancer Therapy: The Negative Impact of PD-L1/PD-1

2021 ◽  
Vol 12 ◽  
Author(s):  
Hao Cai ◽  
Yichi Zhang ◽  
Jian Wang ◽  
Jinyang Gu
Keyword(s):  
Cancer Therapy ◽  
Negative Impact ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
M2 Macrophages ◽  
M1 Macrophages ◽  
Programmed Death ◽  
Antigen Presenting ◽  
Cell Death Protein ◽  
Alternatively Activated

Classically activated M1 macrophages and alternatively activated M2 macrophages are two polarized subsets of macrophages at the extreme ends of a constructed continuum. In the field of cancer research, M2 macrophage reprogramming is defined as the repolarization of pro-tumoral M2 to anti-tumoral M1 macrophages. It is known that colony-stimulating factor 1 (CSF1)/CSF1 receptor (CSF1R) and CSF2/CSF2R signaling play important roles in macrophage polarization. Targeting CSF1/CSF1R for M2 macrophage reprogramming has been widely performed in clinical trials for cancer therapy. Other targets for M2 macrophage reprogramming include Toll-like receptor 7 (TLR7), TLR8, TLR9, CD40, histone deacetylase (HDAC), and PI3Kγ. Although macrophages are involved in innate and adaptive immune responses, M1 macrophages are less effective at phagocytosis and antigen presenting, which are required properties for the activation of T cells and eradication of cancer cells. Similar to T and dendritic cells, the “functionally exhausted” status might be attributed to the high expression of programmed death-ligand 1 (PD-L1) or programmed cell death protein 1 (PD-1). PD-L1 is expressed on both M1 and M2 macrophages. Macrophage reprogramming from M2 to M1 might increase the expression of PD-L1, which can be transcriptionally activated by STAT3. Macrophage reprogramming or PD-L1/PD-1 blockade alone is less effective in the treatment of most cancers. Since PD-L1/PD-1 blockade could make up for the defect in macrophage reprogramming, the combination of macrophage reprogramming and PD-L1/PD-1 blockade might be a novel treatment strategy for cancer therapy.

Do Infarcts Really Expand or Compact? Relationship Between Changing Material Properties and Apparent Infarct Remodeling

2013 ◽  
Author(s):  
William J. Richardson ◽  
Jeffrey W. Holmes
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Cardiac Function ◽  
Material Properties ◽  
Scar Tissue ◽  
Remote Myocardium ◽  
Mortality And Morbidity ◽  
Risk Of Progression ◽  
New Americans ◽  
Compact Relationship

Myocardial infarction (MI) is a leading cause of mortality and morbidity with over 600,000 new Americans suffering an MI each year [1]. Following infarction, damaged muscle is gradually replaced by collagenous scar tissue, while undamaged (remote) myocytes remodel due to altered load. Remodeling of both the infarcted and remote myocardium are important determinants of cardiac function and the risk of progression to heart failure.

Sign in / Sign up

Export Citation Format

Share Document