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Mechanisms of Ageing and Development Jul 2018Here we show that a labyrinth channel compartment and slit diaphragms, which are the histological structures enabling insect nephrocytes ultrafiltration, are established...
Here we show that a labyrinth channel compartment and slit diaphragms, which are the histological structures enabling insect nephrocytes ultrafiltration, are established during embryogenesis first by the garland nephrocytes (GCNs). The later pericardial nephrocytes, which represent the majority of functional nephrocytes in larvae and adults, lack these characteristic features at the embryonic stage. During larval development, a subpopulation of the pericardial cells survives and matures into functional nephrocytes (PCNs) displaying a fully differentiated slit diaphragm and a labyrinth channel compartment. Likely the embryonic pericardial cells have primary functions other than ultrafiltration (e.g. in production and secretion of ECM constituents). We also show, for the first time, that PCNs in the adult fly undergo dramatic histological degeneration upon ageing. The slit diaphragms disappear, the labyrinth channel system degenerates and the lysosomal compartment becomes highly enriched with electron-dense material. When using nephrocytes as a model for genetic screening purposes or to investigate the specific role of genes involved in endocytosis, histological changes occurring upon ageing need to be taken into account when interpreting structural data.
Topics: Aging; Animals; Drosophila melanogaster; Endocytosis; Lysosomes; Pericardium
PubMed: 29702130
DOI: 10.1016/j.mad.2018.04.006 -
Trends in Endocrinology and Metabolism:... Nov 2011Epicardial adipose tissue is an unusual visceral fat depot with anatomical and functional contiguity to the myocardium and coronary arteries. Under physiological... (Review)
Review
Epicardial adipose tissue is an unusual visceral fat depot with anatomical and functional contiguity to the myocardium and coronary arteries. Under physiological conditions, epicardial adipose tissue displays biochemical, mechanical and thermogenic cardioprotective properties. Under pathological circumstances, epicardial fat can locally affect the heart and coronary arteries through vasocrine or paracrine secretion of proinflammatory cytokines. What influences this equilibrium remains unclear. Improved local vascularization, weight loss, and targeted pharmaceutical interventions could help to return epicardial fat to its physiological role. This review focuses on the emerging physiological and pathophysiological aspects of the epicardial fat and its numerous and innovative clinical applications. Particular emphasis is placed on the paracrine/endocrine properties of epicardial fat and its role in the development and progression of atherosclerosis.
Topics: Adipose Tissue; Animals; Atherosclerosis; Humans; Pericardium
PubMed: 21852149
DOI: 10.1016/j.tem.2011.07.003 -
Journal of the American College of... Feb 1986
Topics: Heart; Humans; Methods; Pericardium; Pressure; Surface Properties
PubMed: 3944350
DOI: 10.1016/s0735-1097(86)80497-1 -
Journal of Thoracic Oncology : Official... Apr 2016This article reviews the nomenclature of benign and malignant neoplasm of the heart and pericardium in the 4th edition of the World Health Organization's Classification,... (Review)
Review
This article reviews the nomenclature of benign and malignant neoplasm of the heart and pericardium in the 4th edition of the World Health Organization's Classification, with emphasis on differences since the 3rd edition of 2004. The tumours are divided into benign, malignant, and intermediate tumors of uncertain behavior, with separate sections on germ cell tumours and tumors of the pericardium. There are important updates in the sarcoma classification, with emphasis on the most common site, the left atrium. The importance of the new genetic finding in cardiac myxomas, namely somatic mutations in the PRKAR1A gene underscores the importance of this alteration in the pathogenesis of these tumors. Challenges on the classification of each entity are discussed.
Topics: Heart Neoplasms; Humans; Pericardium; World Health Organization
PubMed: 26725181
DOI: 10.1016/j.jtho.2015.11.009 -
JACC. Heart Failure Jul 2019The elastic pericardium exerts a compressive contact force on the surface of the myocardium that becomes more substantial when heart volume increases, as in patients... (Review)
Review
The elastic pericardium exerts a compressive contact force on the surface of the myocardium that becomes more substantial when heart volume increases, as in patients with various forms of heart failure (HF). Pericardial restraint plays an important role in determining hemodynamics and ventricular function in both health and disease. This review discusses the physiology of pericardial restraint in HF and explores the question of whether it can be targeted indirectly through medical interventions or directly through a number of existing and future therapies.
Topics: Atrial Pressure; Cardiac Resynchronization Therapy; Diuretics; Heart Failure; Hemodynamics; Humans; Pericardiectomy; Pericardium; Stroke Volume; Vasodilator Agents; Ventricular Pressure; Ventricular Remodeling
PubMed: 31248569
DOI: 10.1016/j.jchf.2019.03.021 -
Environmental Toxicology and... Jan 2022Triphenyl phosphate (TPHP) is an organophosphate ester-based plasticizer and flame retardant. The objective of this study was to identify the potential role of epidermal...
Triphenyl phosphate (TPHP) is an organophosphate ester-based plasticizer and flame retardant. The objective of this study was to identify the potential role of epidermal ionocytes in mediating TPHP-induced pericardial edema within zebrafish embryos. Exposure to TPHP from 24 to 72 h post fertilization (hpf) resulted in a significant increase in pericardial edema and the number of ionocytes at 72 hpf relative to time-matched embryos treated with vehicle. In addition, co-exposure of embryos to mannitol (an osmotic diuretic) blocked TPHP-induced pericardial edema and effects on ionocyte abundance. However, knockdown of ATPase1a1.4 - an abundant Na/K-ATPase localized to epidermal ionocytes - mitigated TPHP-induced effects on ionocyte abundance but not pericardial edema, whereas co-exposure of embryos to ouabain - a Na/K-ATPase inhibitor - enhanced TPHP-induced pericardial edema but not ionocyte abundance. Overall, our findings suggest that TPHP may have multiple mechanisms of toxicity leading to an increase in ionocyte abundance and pericardial edema within developing zebrafish embryos.
Topics: Animals; Edema; Embryo, Nonmammalian; Epidermal Cells; Flame Retardants; Organophosphates; Pericardium; Zebrafish
PubMed: 34798236
DOI: 10.1016/j.etap.2021.103776 -
The Journal of Thoracic and... Oct 2018Intrapericardial fibrous adhesions increase the risk of sternal reentry. Proteoglycan 4/lubricin (PRG4) is a mucin-like glycoprotein that lubricates tissue compartments...
OBJECTIVE
Intrapericardial fibrous adhesions increase the risk of sternal reentry. Proteoglycan 4/lubricin (PRG4) is a mucin-like glycoprotein that lubricates tissue compartments and prevents inflammation. We characterized PRG4 expression in human pericardium and examined its effects in vitro on human cardiac myofibroblast fibrotic activity and in vivo as a measure of its therapeutic potential to prevent adhesions.
METHODS
Full-length PRG4 expression was determined using Western blot analysis and amplified luminescent proximity homogeneous assay in human pericardial tissues obtained at cardiotomy. The in vitro effects of PRG4 were investigated on human cardiac myofibroblasts for cell adhesion, collagen gel contraction, and cell-mediated extracellular matrix remodeling. The influence of PRG4 on pericardial homeostasis was determined in a chronic porcine animal model.
RESULTS
PRG4 is expressed in human pericardial fluid and colocalized with pericardial mesothelial cells. Recombinant human PRG4 prevented human cardiac myofibroblast attachment and reduced myofibroblast activity assessed using collagen gel contraction assay (64.6% ± 8.1% vs 47.1% ± 6.8%; P = .02). Using a microgel assay, human cardiac myofibroblast mediated collagen fiber remodeling was attenuated by PRG4 (1.17 ± 0.03 vs 0.90 ± 0.05; P = .002). In vivo, removal of pericardial fluid alone induced severe intrapericardial adhesion formation, tissue thickening, and inflammatory fluid collections. Restoration of intrapericardial PRG4 was protective against fibrous adhesions and preserved the pericardial space.
CONCLUSIONS
For the first time, we show that PRG4 is expressed in human pericardial fluid and regulates local fibrotic myofibroblast activity. Loss of PRG4-enriched pericardial fluid after cardiotomy might induce adhesion formation. Therapeutic restoration of intrapericardial PRG4 might prevent fibrous/inflammatory adhesions and reduce the risk of sternal reentry.
Topics: Animals; Cell Adhesion; Cells, Cultured; Collagen; Disease Models, Animal; Extracellular Matrix; Humans; Myofibroblasts; Pericardial Fluid; Pericardium; Proteoglycans; Sus scrofa; Thoracic Diseases; Tissue Adhesions
PubMed: 29859675
DOI: 10.1016/j.jtcvs.2018.03.170 -
Wound Repair and Regeneration :... 2012Cardiovascular disease is the leading cause of death in the U.S. and worldwide. Failure to properly repair or regenerate damaged cardiac tissues after myocardial... (Review)
Review
Cardiovascular disease is the leading cause of death in the U.S. and worldwide. Failure to properly repair or regenerate damaged cardiac tissues after myocardial infarction is a major cause of heart failure. In contrast to humans and other mammals, zebrafish hearts regenerate after substantial injury or tissue damage. Here, we review recent progress in studying zebrafish heart regeneration, addressing the molecular and cellular responses in the three tissue layers of the heart: myocardium, epicardium, and endocardium. We also compare different injury models utilized to study zebrafish heart regeneration and discuss the differences in responses to injury between mammalian and zebrafish hearts. By learning how zebrafish hearts regenerate naturally, we can better design therapeutic strategies for repairing human hearts after myocardial infarction.
Topics: Animals; Cardiovascular Diseases; Cardiovascular Physiological Phenomena; Cell Proliferation; Endocardium; Heart; Humans; Models, Animal; Myocardium; Myocytes, Cardiac; Pericardium; Regeneration; Zebrafish
PubMed: 22818295
DOI: 10.1111/j.1524-475X.2012.00814.x -
Circulation Research Jun 2012Epithelial to mesenchymal transition (EMT) converts epithelial cells to mobile and developmentally plastic mesenchymal cells. All cells in the heart arise from one or... (Review)
Review
Epithelial to mesenchymal transition (EMT) converts epithelial cells to mobile and developmentally plastic mesenchymal cells. All cells in the heart arise from one or more EMTs. Endocardial and epicardial EMTs produce most of the noncardiomyocyte lineages of the mature heart. Endocardial EMT generates valve progenitor cells and is necessary for formation of the cardiac valves and for complete cardiac septation. Epicardial EMT is required for myocardial growth and coronary vessel formation, and it generates cardiac fibroblasts, vascular smooth muscle cells, a subset of coronary endothelial cells, and possibly a subset of cardiomyocytes. Emerging studies suggest that these developmental mechanisms are redeployed in adult heart valve disease, in cardiac fibrosis, and in myocardial responses to ischemic injury. Redirection and amplification of disease-related EMTs offer potential new therapeutic strategies and approaches for treatment of heart disease. Here, we review the role and molecular regulation of endocardial and epicardial EMT in fetal heart development, and we summarize key literature implicating reactivation of endocardial and epicardial EMT in adult heart disease.
Topics: Animals; Endocardium; Epithelial Cells; Epithelial-Mesenchymal Transition; Heart; Heart Diseases; Humans; Pericardium
PubMed: 22679138
DOI: 10.1161/CIRCRESAHA.111.259960 -
Developmental Cell Mar 2020The epicardium is essential during cardiac development, homeostasis, and repair, and yet fundamental insights into its underlying cell biology, notably epicardium...
The epicardium is essential during cardiac development, homeostasis, and repair, and yet fundamental insights into its underlying cell biology, notably epicardium formation, lineage heterogeneity, and functional cross-talk with other cell types in the heart, are currently lacking. In this study, we investigated epicardial heterogeneity and the functional diversity of discrete epicardial subpopulations in the developing zebrafish heart. Single-cell RNA sequencing uncovered three epicardial subpopulations with specific genetic programs and distinctive spatial distribution. Perturbation of unique gene signatures uncovered specific functions associated with each subpopulation and established epicardial roles in cell adhesion, migration, and chemotaxis as a mechanism for recruitment of leukocytes into the heart. Understanding which mechanisms epicardial cells employ to establish a functional epicardium and how they communicate with other cardiovascular cell types during development will bring us closer to repairing cellular relationships that are disrupted during cardiovascular disease.
Topics: Animals; Cell Lineage; Gene Expression Regulation, Developmental; Pericardium; RNA-Seq; Single-Cell Analysis; Transcriptome; Zebrafish
PubMed: 32084358
DOI: 10.1016/j.devcel.2020.01.023