scholarly journals Epoxyeicosatrienoic Acids Regulate Macrophage Polarization and Prevent LPS-Induced Cardiac Dysfunction

2015 ◽  
Vol 230 (9) ◽  
pp. 2108-2119 ◽  
Author(s):  
Meiyan Dai ◽  
Lujin Wu ◽  
Zuowen He ◽  
Shasha Zhang ◽  
Chen Chen ◽  
...  
Keyword(s):  
Cardiac Dysfunction ◽  
Macrophage Polarization ◽  
Epoxyeicosatrienoic Acids

CLEC5A knockdown protects against the cardiac dysfunction after Myocardial infarction by suppressing macrophage polarization, NLRP3 inflammasome activation and pyroptosis

2021 ◽  
Author(s):  
Xin Wang ◽  
Yu Hu ◽  
Yaguang Wang ◽  
Dapeng Shen ◽  
Guizhou Tao
Keyword(s):  
Myocardial Infarction ◽  
Nlrp3 Inflammasome ◽  
Cardiac Dysfunction ◽  
Macrophage Polarization ◽  
Left Ventricular ◽  
Receptor Protein ◽  
Inflammasome Activation ◽  
M1 Polarization

Increasing evidence has shown that NOD-like receptor protein 3 (NLRP3) inflammasome and pyroptotic cell death play vital roles in the pathophysiology of myocardial infarction (MI), a common cardiovascular disease characterized with cardiac dysfunction. C-type lectin member 5A (CLEC5A) is reported to strongly associate with activation of NLRP3 inflammasome and pyroptosis. In this study, in vivo MI model was established by the ligation of left anterior descending coronary artery on male C57BL/6 mice, and CLEC5A knockdown was further achieved by intra-myocardial injection of adenovirus delivering shRNA-CLEC5A. CLEC5A was found to be highly expressed in left ventricular of MI mice, while CLEC5A knockdown conversely alleviated the cardiac dysfunction in MI mice. Besides, MI-induced classical activation of macrophages was significantly inhibited after CLEC5A silencing. Additionally, CLEC5A knockdown dramatically inhibited MI-triggered activation of NLRP3 inflammasome, pyroptosis and NF-κB signaling in left ventricular of mice. In vitro experiment further validated that CLEC5A knockdown suppressed M1 polarization in LPS/IFNγ-stimulated RAW264.7 cells, and inhibited the polarized RAW264.7-induced activation of NLRP3 inflammasome/pyroptosis signaling in co-cultured cardiomyocytes. In conclusion, CLEC5A knockdown protects against the MI-induced cardiac dysfunction by regulating macrophage polarization, NLRP3 inflammasome and cell pyroptosis.

scholarly journals C1q/TNF‐related protein‐9 promotes macrophage polarization and improves cardiac dysfunction after myocardial infarction

2019 ◽  
Vol 234 (10) ◽  
pp. 18731-18747 ◽  
Author(s):  
Mingxin Liu ◽  
Lin Yin ◽  
Wei Li ◽  
Juan Hu ◽  
Huibo Wang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Dysfunction ◽  
Macrophage Polarization ◽  
Related Protein

scholarly journals Harmine Alleviated Sepsis-Induced Cardiac Dysfunction by Modulating Macrophage Polarization via the STAT/MAPK/NF-κB Pathway

2022 ◽  
Vol 9 ◽  
Author(s):  
Weibin Ruan ◽  
Xinyun Ji ◽  
Yating Qin ◽  
Xinxin Zhang ◽  
Xiaoning Wan ◽  
...  
Keyword(s):  
Cardiac Dysfunction ◽  
Macrophage Polarization ◽  
Raw 264.7 Cells ◽  
Drug Induced ◽  
M1 Polarization ◽  
M1 Phenotype ◽  
Phenotype Markers ◽  
Cox 2 ◽  
Underlying Mechanisms

Sepsis is a dysregulated systemic inflammatory response that often leads to cardiac dysfunction, which is termed sepsis-induced cardiomyopathy (SIC). Harmine, a natural β-carboline alkaloid compound, has been shown to exert pharmacological effects on several diseases. Here, we investigated whether harmine protected against SIC development and the underlying mechanisms. In vitro, the expression of the M1 phenotype markers iNOS and COX-2 was increased in RAW 264.7 cells stimulated with lipopolysaccharide (LPS), but this effect was reversed by the harmine intervention. Furthermore, LPS-induced increases in the levels of inflammatory cytokines, including IL-1β, IL-6, TNF-α, iNOS, COX-2, PGE2 and TXB2, generated by macrophages were suppressed when the cells were pretreated with harmine. Meanwhile, our findings showed that harmine administration effectively attenuated inflammation and apoptosis in H9c2 cells in the proinflammatory environment produced by macrophages, as evidenced by reductions in NLRP3 and cleaved caspase 3 levels and the p-NF-κB/NF-κB ratio. The western blot results indicated that the mechanisms underlying harmine-mediated inhibition of M1 polarization might be associated with suppression of STAT1/3, NF-κB and MAPK activation. Furthermore, an LPS injection induced cardiac dysfunction and decreased the survival rate of mice, which were alleviated by harmine treatment, and the relevant mechanism was possibly attributed to a drug-induced attenuation of the inflammatory and apoptotic processes in cardiomyocytes. Collectively, these results implied that harmine treatment protected against SIC by suppressing M1 phenotypic polarization and inflammation in macrophages.

Local production of tenascin-C acts as a trigger for monocyte/macrophage recruitment that provokes cardiac dysfunction

2017 ◽  
Vol 114 (1) ◽  
pp. 123-137 ◽  
Author(s):  
Dounia Abbadi ◽  
Fanny Laroumanie ◽  
Mathilde Bizou ◽  
Joffrey Pozzo ◽  
Danièle Daviaud ◽  
...  
Keyword(s):  
Cardiac Dysfunction ◽  
Immune Cell ◽  
Inflammatory Diseases ◽  
Macrophage Polarization ◽  
Systolic Dysfunction ◽  
Cardiac Cells ◽  
Macrophage Migration ◽  
Signal Molecule ◽  
Inflammatory Microenvironment ◽  
Tenascin C

Abstract Aims Tenascin-C (TNC) is an endogenous danger signal molecule strongly associated with inflammatory diseases and with poor outcome in patients with cardiomyopathies. Its function within pathological cardiac tissue during pressure overload remains poorly understood. Methods and results We showed that TNC accumulates after 1 week of transverse aortic constriction (TAC) in the heart of 12-week-old male mice. By cross bone marrow transplantation experiments, we determined that TNC deposition relied on cardiac cells and not on haematopoietic cells. The expression of TNC induced by TAC, or by administration of a recombinant lentivector coding for TNC, triggered a pro-inflammatory cardiac microenvironment, monocyte/macrophage (MO/MΦ) accumulation, and systolic dysfunction. TNC modified macrophage polarization towards the pro-inflammatory phenotype and stimulated RhoA/Rho-associated protein kinase (ROCK) pathways to promote mesenchymal to amoeboid transition that enhanced macrophage migration into fibrillar collagen matrices. The amplification of inflammation and MO/MΦ recruitment by TNC was abrogated by genetic invalidation of TNC in knockout mice. These mice showed less ventricular remodelling and an improved cardiac function after TAC as compared with wild-type mice. Conclusions By promoting a pro-inflammatory microenvironment and macrophage migration, TNC appears to be a key factor to enable the MO/MΦ accumulation within fibrotic hearts leading to cardiac dysfunction. As TNC is highly expressed during inflammation and sparsely during the steady state, its inhibition could be a promising therapeutic strategy to control inflammation and immune cell infiltration in heart disease.

Pulmonary Edema and Simultaneous Cardiac Dysfunction After Epileptic Seizures

2013 ◽  
Vol 40 (06) ◽  
pp. 896-897
Author(s):  
V. Pelliccia ◽  
C. Pizzanelli ◽  
S. Pini ◽  
P. Malacarne ◽  
U. Bonuccelli
Keyword(s):  
Pulmonary Edema ◽  
Cardiac Dysfunction ◽  
Epileptic Seizures

Plasma amino-terminal pro-brain natriuretic peptide: A novel approach to the diagnosis of cardiac dysfunction

2000 ◽  
Vol 6 (2) ◽  
pp. 130-139 ◽  
Author(s):  
Duncan J. Campbell ◽  
Kenneth I. Mitchelhill ◽  
Stephen M. Schlicht ◽  
Russell J. Booth
Keyword(s):  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Cardiac Dysfunction ◽  
Amino Terminal ◽  
Novel Approach
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