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Trends in Cell Biology Apr 2020The positioning of nuclei within the cell is a dynamic process that depends on the cell's fate and developmental stage and that is adjusted for optimal cell function.... (Review)
Review
The positioning of nuclei within the cell is a dynamic process that depends on the cell's fate and developmental stage and that is adjusted for optimal cell function. This is especially true in skeletal muscle cells, which contain hundreds of myonuclei distributed evenly along the periphery of the muscle cell. Mispositioned myonuclei are often associated with muscle dysfunction and disease. Different mechanisms governing myonuclear positioning are now emerging, with several of the new genes implicated in nuclear movement linked to human muscle disease. Here we discuss the recent advances in myonuclear positioning and its implications for muscle size and function from the view of Drosophila. Additionally, we highlight similarities and differences to mammalian systems and provide connections to human muscle disease.
Topics: Animals; Cell Nucleus; Drosophila melanogaster; Humans; Movement; Muscle Cells; Muscle, Skeletal
PubMed: 32008895
DOI: 10.1016/j.tcb.2020.01.002 -
Redox Biology 2015Autophagy regulates the metabolism, survival, and function of numerous cell types, including those comprising the cardiovascular system. In the vasculature, changes in... (Review)
Review
Autophagy regulates the metabolism, survival, and function of numerous cell types, including those comprising the cardiovascular system. In the vasculature, changes in autophagy have been documented in atherosclerotic and restenotic lesions and in hypertensive vessels. The biology of vascular smooth muscle cells appears particularly sensitive to changes in the autophagic program. Recent evidence indicates that stimuli or stressors evoked during the course of vascular disease can regulate autophagic activity, resulting in modulation of VSMC phenotype and viability. In particular, certain growth factors and cytokines, oxygen tension, and pharmacological drugs have been shown to trigger autophagy in smooth muscle cells. Importantly, each of these stimuli has a redox component, typically associated with changes in the abundance of reactive oxygen, nitrogen, or lipid species. Collective findings support the hypothesis that autophagy plays a critical role in vascular remodeling by regulating smooth muscle cell phenotype transitions and by influencing the cellular response to stress. In this graphical review, we summarize current knowledge on the role of autophagy in the biology of the smooth muscle cell in (patho)physiology.
Topics: Atherosclerosis; Autophagy; Humans; Lipid Metabolism; Muscle, Smooth, Vascular; Myocytes, Smooth Muscle; Oxidative Stress
PubMed: 25544597
DOI: 10.1016/j.redox.2014.12.007 -
Cardiovascular Research Mar 2018
Topics: Animals; Calcium Signaling; Cell Lineage; Cell Movement; Cell Plasticity; Cell Proliferation; Humans; Muscle, Smooth, Vascular; Myocytes, Smooth Muscle; Neovascularization, Physiologic; Phenotype; Vascular Diseases; Vasoconstriction; Vasodilation
PubMed: 29408963
DOI: 10.1093/cvr/cvy031 -
Current Opinion in Immunology Feb 2016Alarmins are a heterogeneous group of endogenous molecules that signal cellular damage when sensed extracellularly. Heme is an endogenous molecule that acts as a... (Review)
Review
Alarmins are a heterogeneous group of endogenous molecules that signal cellular damage when sensed extracellularly. Heme is an endogenous molecule that acts as a prosthetic group of hemoproteins, such as hemoglobin and myoglobin. When released from damaged red blood cells or muscle cells, oxidized hemoglobin and myoglobin release their prosthetic heme groups, respectively. This generates labile heme, which is sensed by pattern recognition receptors (PRR) expressed by innate immune cells and possibly regulatory T cells (TREG). The ensuing adaptive response, which alerts for the occurrence of red blood cell or muscle cell damage, regulates the pathologic outcome of hemolysis or rhabdomyolysis, respectively. In conclusion, we propose that labile heme is an alarmin.
Topics: Adaptive Immunity; Alarmins; Animals; Endothelial Cells; Erythrocytes; Gene Expression Regulation; Heme; Humans; Immunity, Innate; Macrophages; Muscle Cells; Neutrophils; Reactive Oxygen Species; Receptors, Pattern Recognition; Signal Transduction
PubMed: 26741528
DOI: 10.1016/j.coi.2015.11.006 -
Nitric Oxide : Biology and Chemistry Jul 2018Nitric oxide-sensitive guanylyl cyclase (NO-GC) has been shown to regulate a plethora of different functions in the body. These include, among many others, the... (Review)
Review
Nitric oxide-sensitive guanylyl cyclase (NO-GC) has been shown to regulate a plethora of different functions in the body. These include, among many others, the fine-tuning of vascular tone, platelet reactivity and gastrointestinal motility. Evidence for the participation of NO-GC in these functions has been obtained from various species including humans, rodents, as well as insects. Clearly, individual cell types that express NO-GC contribute differentially to organ-specific NO/cGMP signaling in the body. Hence, identification of NO-GC-expressing cells and their individual involvement in NO/cGMP signaling constituted the focus of many studies over the last 40 years. Probably most information has been obtained from vascular smooth muscle cells and platelets, in which NO-GC is known to induce relaxation and inhibition of aggregation, respectively. Many other cell types that express the enzyme have been linked to certain functions, e.g. cardiomyocyte/inotropy or gastrointestinal smooth muscle cells/motility. However, in some cell types, e.g. myofibroblasts or pericytes, NO-GC expression is evident but individual functions of NO/cGMP signaling have yet to be assigned, whereas in other cell types, e.g. in erythrocytes, expression and role of NO-GC is still a matter of debate. This review discusses the current knowledge on 'less popular' cell types that express NO-GC (pericytes, myofibroblasts, cardiomyocytes, adipocytes, interstitial cells of Cajal, fibroblast-like cells and blood cells) and outlines possible further functions in cell types that have not gained strong attention so far.
Topics: Adipocytes; Animals; Fibroblasts; Humans; Interstitial Cells of Cajal; Myocytes, Cardiac; Myocytes, Smooth Muscle; Myofibroblasts; Pericytes; Signal Transduction; Soluble Guanylyl Cyclase
PubMed: 29626542
DOI: 10.1016/j.niox.2018.03.020 -
Frontiers in Immunology 2020The pathobiology of atherosclerotic disease requires further elucidation to discover new approaches to address its high morbidity and mortality. To date, over 17 million... (Review)
Review
The pathobiology of atherosclerotic disease requires further elucidation to discover new approaches to address its high morbidity and mortality. To date, over 17 million cardiovascular-related deaths have been reported annually, despite a multitude of surgical and nonsurgical interventions and advances in medical therapy. Existing strategies to prevent disease progression mainly focus on management of risk factors, such as hypercholesterolemia. Even with optimum current medical therapy, recurrent cardiovascular events are not uncommon in patients with atherosclerosis, and their incidence can reach 10-15% per year. Although treatments targeting inflammation are under investigation and continue to evolve, clinical breakthroughs are possible only if we deepen our understanding of vessel wall pathobiology. Vascular smooth muscle cells (VSMCs) are one of the most abundant cells in vessel walls and have emerged as key players in disease progression. New technologies, including hybridization proximity ligation assays, cell fate tracing with the CreER-loxP system and single-cell sequencing technology with spatial resolution, broaden our understanding of the complex biology of these intriguing cells. Our knowledge of contractile and synthetic VSMC phenotype switching has expanded to include macrophage-like and even osteoblast-like VSMC phenotypes. An increasing body of data suggests that VSMCs have remarkable plasticity and play a key role in cell-to-cell crosstalk with endothelial cells and immune cells during the complex process of inflammation. These are cells that sense, interact with and influence the behavior of other cellular components of the vessel wall. It is now more obvious that VSMC plasticity and the ability to perform nonprofessional phagocytic functions are key phenomena maintaining the inflammatory state and senescent condition and actively interacting with different immune competent cells.
Topics: Animals; Atherosclerosis; Humans; Inflammation; Muscle, Smooth, Vascular; Myocytes, Smooth Muscle; Vasculitis
PubMed: 33324416
DOI: 10.3389/fimmu.2020.599415 -
Applied Microbiology and Biotechnology Sep 2014Animal cell culture is a highly complex process, in which cells are grown under specific conditions. The growth and development of these cells is a highly unnatural... (Review)
Review
Animal cell culture is a highly complex process, in which cells are grown under specific conditions. The growth and development of these cells is a highly unnatural process in vitro condition. Cells are removed from animal tissues and artificially cultured in various culture vessels. Vitamins, minerals, and serum growth factors are supplied to maintain cell viability. Obtaining result homogeneity of in vitro and in vivo experiments is rare, because their structure and function are different. Living tissues have highly ordered complex architecture and are three-dimensional (3D) in structure. The interaction between adjacent cell types is quite distinct from the in vitro cell culture, which is usually two-dimensional (2D). Co-culture systems are studied to analyze the interactions between the two different cell types. The muscle and fat co-culture system is useful in addressing several questions related to muscle modeling, muscle degeneration, apoptosis, and muscle regeneration. Co-culture of C2C12 and 3T3-L1 cells could be a useful diagnostic tool to understand the muscle and fat formation in animals. Even though, co-culture systems have certain limitations, they provide a more realistic 3D view and information than the individual cell culture system. It is suggested that co-culture systems are useful in evaluating the intercellular communication and composition of two different cell types.
Topics: Adipocytes; Animals; Coculture Techniques; Muscle Cells
PubMed: 25038928
DOI: 10.1007/s00253-014-5935-9 -
Current Topics in Membranes 2020Vascular smooth muscle cells (VSMC) are now considered important contributors to the pathophysiological and biophysical mechanisms underlying arterial stiffening in... (Review)
Review
Vascular smooth muscle cells (VSMC) are now considered important contributors to the pathophysiological and biophysical mechanisms underlying arterial stiffening in aging. Here, we review mechanisms whereby VSMC stiffening alters vascular function and contributes to the changes in vascular stiffening observed in aging and cardiovascular disease. Vascular stiffening in arterial aging was historically associated with changes in the extracellular matrix; however, new evidence suggests that endothelial and vascular smooth muscle cell stiffness also contribute to overall blood vessel stiffness. Furthermore, VSMC play an integral role in regulating matrix deposition and vessel wall contractility via interaction between the actomyosin contractile unit and adhesion structures that anchor the cell within the extracellular matrix. Aged-induce phenotypic modulation of VSMC from a contractile to a synthetic phenotype is associated with decreased cellular contractility and increased cell stiffness. Aged VSMC also display reduced mechanosensitivity and adaptation to mechanical signals from their microenvironment due to impaired intracellular signaling. Finally, evidence for decreased contractility in arteries from aged animals demonstrate that changes at the cellular level result in decreased functional properties at the tissue level.
Topics: Aging; Animals; Extracellular Matrix; Muscle, Smooth, Vascular; Myocytes, Smooth Muscle; Vascular Stiffness
PubMed: 33837694
DOI: 10.1016/bs.ctm.2020.08.008 -
Journal of Muscle Research and Cell... Jun 2019Vascular smooth muscle cells (VSMCs) are the predominant cell type in the blood vessel wall and normally adopt a quiescent, contractile phenotype. VSMC migration is... (Review)
Review
Vascular smooth muscle cells (VSMCs) are the predominant cell type in the blood vessel wall and normally adopt a quiescent, contractile phenotype. VSMC migration is tightly controlled, however, disease associated changes in the soluble and insoluble environment promote VSMC migration. Classically, studies investigating VSMC migration have described the influence of soluble factors. Emerging data has highlighted the importance of insoluble factors, including extracellular matrix stiffness and porosity. In this review, we will recap on the important signalling pathways that regulate VSMC migration and reflect on the potential importance of emerging regulators of VSMC function.
Topics: Animals; Cell Movement; Extracellular Matrix; Humans; Muscle, Smooth, Vascular; Myocytes, Smooth Muscle
PubMed: 31254136
DOI: 10.1007/s10974-019-09531-z -
Current Osteoporosis Reports Oct 2019Bone and muscle mass increase in response to mechanical loading and biochemical cues. Bone-forming osteoblasts differentiate into early osteocytes which ultimately... (Review)
Review
PURPOSE OF REVIEW
Bone and muscle mass increase in response to mechanical loading and biochemical cues. Bone-forming osteoblasts differentiate into early osteocytes which ultimately mature into late osteocytes encapsulated in stiff calcified matrix. Increased muscle mass originates from muscle stem cells (MuSCs) enclosed between their plasma membrane and basal lamina. Stem cell fate and function are strongly determined by physical and chemical properties of their microenvironment, i.e., the cell niche.
RECENT FINDINGS
The cellular niche is a three-dimensional structure consisting of extracellular matrix components, signaling molecules, and/or other cells. Via mechanical interaction with their niche, osteocytes and MuSCs are subjected to mechanical loads causing deformations of membrane, cytoskeleton, and/or nucleus, which elicit biochemical responses and secretion of signaling molecules into the niche. The latter may modulate metabolism, morphology, and mechanosensitivity of the secreting cells, or signal to neighboring cells and cells at a distance. Little is known about how mechanical loading of bone and muscle tissue affects osteocytes and MuSCs within their niches. This review provides an overview of physicochemical niche conditions of (early) osteocytes and MuSCs and how these are sensed and determine cell fate and function. Moreover, we discuss how state-of-the-art imaging techniques may enhance our understanding of these conditions and mechanisms.
Topics: Animals; Cell Differentiation; Extracellular Matrix; Humans; Mechanotransduction, Cellular; Muscle Cells; Osteocytes; Stress, Mechanical
PubMed: 31428977
DOI: 10.1007/s11914-019-00522-0