Role of Exosomes in Myocardial Remodeling

Waldenström, Anders; Ronquist, Gunnar

doi:10.1161/circresaha.114.300584

Cited by 137 publications

(97 citation statements)

References 135 publications

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“…17 Prostasomes share cholesterol-and sphingomyelin-rich plasma membranes 20 with other exosomes secreted by pancreatic, breast, or colon adenocarcinoma cells. 21,22 Here, we identify a novel and unexpected role of the polyP/FXIIdriven intrinsic pathway of coagulation in PC-associated thrombosis. Coagulation analyses of patient plasma and PE models in genetically altered mice show that PC cells and prostasomes expose long-chain polyP on their surface.…”

Section: Introductionmentioning

confidence: 97%

The polyphosphate–factor XII pathway drives coagulation in prostate cancer-associated thrombosis

Nickel

Ronquist

Länger

et al. 2015

Blood

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126

111

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Section: Introductionmentioning

confidence: 97%

The polyphosphate–factor XII pathway drives coagulation in prostate cancer-associated thrombosis

Nickel

Ronquist

Länger

et al. 2015

Blood

Self Cite

126

111

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“…3,4 Exosomes are membranous vesicles with a diameter <100 nM. 5,6 They are mainly formed from the inward budding of multi-vesicular bodies and are shed from both healthy and diseased cells. 7 Exosomes contain abundant miRNAs, mRNAs, proteins, or even organelles derived from donor cells that are transferred into specific target cells.…”

Section: Introductionmentioning

confidence: 99%

Macrophage-Derived mir-155-Containing Exosomes Suppress Fibroblast Proliferation and Promote Fibroblast Inflammation during Cardiac Injury

et al. 2017

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Inflammation plays an important role in cardiac injuries. Here, we examined the role of miRNA in regulating inflammation and cardiac injury during myocardial infarction. We showed that mir-155 expression was increased in the mouse heart after myocardial infarction. Upregulated mir-155 was primarily presented in macrophages and cardiac fibroblasts of injured hearts, while pri-mir-155 was only expressed in macrophages. mir-155 was also presented in exosomes derived from macrophages, and it can be transferred into cardiac fibroblasts by macrophagederived exosomes. A mir-155 mimic or mir-155 containing exosomes inhibited cardiac fibroblast proliferation by downregulating Son of Sevenless 1 expression and promoted inflammation by decreasing Suppressor of Cytokine Signaling 1 expression. These effects were reversed by the addition of a mir-155 inhibitor. In vivo, mir-155-deficient mice showed a significant reduction of the incidence of cardiac rupture and an improved cardiac function compared with wild-type mice. Moreover, transfusion of wild-type macrophage exosomes to mir-155 À/À mice exacerbated cardiac rupture. Finally, the mir-155-deficient mice exhibited elevated fibroblast proliferation and collagen production, along with reduced cardiac inflammation in injured heart. Taken together, our results demonstrate that activated macrophages secrete mir-155-enriched exosomes and identify macrophagederived mir-155 as a paracrine regulator for fibroblast proliferation and inflammation; thus, a mir-155 inhibitor (i.e., mir-155 antagomir) has the potential to be a therapeutic agent for reducing acute myocardial-infarction-related adverse events.

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“…Exosomes can be taken up by neighbouring or distant cells and can be functional in the recipient cells by fusion with the plasma membrane, via receptor-mediated uptake or by internalisation via endocytosis or macropinocytosis [87]. Since the discovery of miRNA in exosomes, a number of studies have focused on the identification and function of exosomal miRNAs in cancer [88] and cardiovascular diseases [89][90][91][92][93]. Interestingly, cancer cell and mechanisms used by lncRNAs are much more complex and diversified than miRNAs [115].…”

Section: Vascular Cell-to-cell Communication Through Mirnasmentioning

confidence: 99%

Role of noncoding RNA in vascular remodelling

Lin

Bradshaw

Baker

2016

Current Opinion in Lipidology

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Purpose of review: Non-coding RNA (ncRNAs), such as microRNAs (miRNAs) and long non-coding RNAs (LncRNAs), are becoming fundamentally important in the pathophysiology relating to injury-induced vascular remodelling. We highlight recent studies that demonstrate the involvement of ncRNAs in vein graft disease, in in-stent restenosis (ISR) and in pulmonary arterial hypertension (PAH), with a particular focus on endothelial cell (EC) and vascular smooth muscle cell (VSMC) function. We also briefly discuss the emerging role of exosomal-derived ncRNAs and how this mechanism impacts on vascular function.

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Role of Exosomes in Myocardial Remodeling

Cited by 137 publications

References 135 publications

The polyphosphate–factor XII pathway drives coagulation in prostate cancer-associated thrombosis

The polyphosphate–factor XII pathway drives coagulation in prostate cancer-associated thrombosis

Macrophage-Derived mir-155-Containing Exosomes Suppress Fibroblast Proliferation and Promote Fibroblast Inflammation during Cardiac Injury

Role of noncoding RNA in vascular remodelling

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