China
Africa
Explore chapters and articles related to this topic
Functional Properties of Muscle
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
Smooth muscle cells are relatively small and spindle-shaped, being 2–10 µm in diameter 20–500 µm in length, with a single nucleus (Figure 10.22). Smooth muscle is so called because it is non-striated, the thick and thin filaments are not organized into myofibrils, and there are no aligned sarcomeres to produce striations. Instead, the thick filaments are scattered throughout the cell, and the organization of their myosin is different from that in skeletal and cardiac muscle. The thin filaments are connected to dense bodies, which are functionally similar to the Z discs of skeletal muscle. The dense bodies are part of a filamentous network that is firmly attached to the cell membrane and composed mainly of the protein desmin. Thus, when the thick and thin filaments slide past one another, force is transmitted to the cell membrane. However, the unorganized arrangement of thick and thin filaments allows the development of force over a range of lengths that can be four times that in skeletal muscle. The amount of myosin in smooth muscle, in mg/g of muscle, is roughly a third to a quarter of that in skeletal muscle, while the amount of actin can be up to twice as much.
The cell and tissues
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
ATP is required to fuel: Energy production itself. It is necessary to initiate glycolysis and fatty acid oxidation.Active transport of electrolytes across the plasma membrane, e.g., the Na+/K+ pump that restores the resting potential of the heart’s pacemaker cells.The amplification of the second messenger systems in cells. This process involves small amounts of signalling molecules (for example, water soluble hormones and neurotransmitters) attaching to the surface of the cell and initiating a process involving a number of membrane and intracellular proteins, that amplify the message to ensure that there is a sufficient response within the cell. This means that a relatively weak signal can produce a significant cellular action. The amino acid endocrines, such as antidiuretic hormone, function in this way.Contraction of skeletal, cardiac and smooth muscle cells.Phosphorylation of molecules to enable and enhance reactions in the cell.
Assessment of Airway Smooth Muscle Growth and Division: In Vitro Studies
Published in Alastair G. Stewart, AIRWAY WALL REMODELLING in ASTHMA, 2020
The ability of smooth muscle cells in culture to contract or relax in response to specific agonists is well documented.20,21 Airway smooth muscle cells in culture are no exception to this. Avner et al.15 reported that subconfluent primary cultures of canine tracheal smooth muscle cells contracted in response to the cholinomimetic carbachol. Contraction, however, in cultured smooth muscle cells is dependent upon a number of carefully defined culture conditions.
Airway smooth muscle in contractility and remodeling of asthma: potential drug target mechanisms
Published in Expert Opinion on Therapeutic Targets, 2023
Latifa Khalfaoui, Christina M. Pabelick
Inhaled corticosteroids (ICSs) and β2-adrenergic receptor agonists remain mainstays of asthma therapy [157] and are clinically effective in most patients [158]. However, some asthmatic patients remain at high risk of severe exacerbation, hospitalization, and mortality [159]. Anti-inflammatory agents or anticholinergics indirectly target smooth muscle cell dysfunction [160]. Bronchial thermoplasty targets ASM directly by reducing smooth muscle mass, although the mechanisms of action and long-term side effects are still unclear [161]. Monoclonal antibodies such as omalizumab, mepolizumab, benralizumab, dupilumab, and tezepelumab have been approved by the FDA and given their targeting of key inflammatory pathways such as IL4, IL-13, and TSLP, they should be effective in modulating ASM contractility in the context of AHR [162]. Whether they will be as effective in targeting remodeling remains less clear given (as summarized briefly earlier) the contribution of different inflammatory pathways in different cell types change during the course and severity of disease. Thus, the field remains open for targeting non-immune or non-inflammatory pathways in asthma. Here, we believe the ASM (among other cell types) is an appealing avenue.
Mechanistic links between systemic hypertension and open angle glaucoma
Published in Clinical and Experimental Optometry, 2022
Ying-kun Cui, Li Pan, Tim Lam, Chun-yi Wen, Chi-wai Do
However, under physiological conditions, there is a lack of a linear relationship between ocular perfusion pressure and ocular blood flow.43 This is attributed to the ability of maintaining a relatively constant ocular blood flow despite fluctuating ocular perfusion pressure, which is known as autoregulation.42 Autoregulation is a complicated process and refers to the intrinsic property of organs to maintain a constant blood flow in response to changes in perfusion pressure. It is controlled by both myogenic and metabolic mechanisms. Since the retina has no autonomic innervation, the blood supply to the inner retina is regulated by local vascular mechanisms. In the myogenic mechanism, the smooth muscle cells in the blood vessels contract when being stretched. This process is possibly mediated by activating voltage-gated Ca2+ channels, resulting in an increased vascular resistance due to vasoconstriction.44
MiRNA: a potential target for gene diagnosis and treatment of atherosclerotic stroke
Published in International Journal of Neuroscience, 2021
Yi. Bao, Sijing. Li, Yayong. Ding, Xinyu. Du, Miao. Zhang, Wanjuan. Tang, Siqin. Zhou
In the aspect of vascular smooth muscle cells, K Knoepp et al. demonstrated that miRNA was involved in the differential gene regulation of vascular remodeling by inducing the formation of neointima through the femoral artery line bundle of C57BL/6 mice, which played a key role in the proliferation of vascular smooth muscle cells and provided a therapeutic target for in-stent restenosis after angioplasty [19]. Previous studies have found that miRNA-29, miRNA-143/145 and miRNA-221/222 are involved in the regulation of phenotypic transformation, proliferation and migration of vascular smooth muscle cells [20]. MiRNA-143/145 is expressed in many pathological and physiological processes and can control the smooth muscle cell phenotype. In the study of pluripotent mouse cardiac progenitor cells, miRNA-145 and miRNA-143 were found to be down-regulated in the injury or atherosclerotic vessels of smooth muscle cells with low proliferation and differentiation. KLF2 is a key regulator of endothelial gene expression patterns that induce atherosclerosis, and binding to the promoter induces a significant up-regulation of miRNA-143/145 clusters [21]. In addition, miRNA-145 and miRNA-143 synergistically target transcription factor networks, including kruppel-like factor 4, myocardin and Elk-1 (members of the ETS oncogene family), which promote the differentiation and proliferation of smooth muscle cells [22].