Omar Khalid
Smooth muscle plasticity refers to the ability of smooth muscle cells to undergo phenotypic switching, converting from a contractile state to a less differentiated state of proliferation, migration, and secretion. This process, known as phenotypic modulation or plasticity, has been observed in smooth muscle cells of the carotid artery following injury. While the specific biochemical cues triggering this modulation remain unclear, it is believed to play a significant role in the development of atherosclerosis, primary pulmonary hypertension, and vascular occlusive diseases. Smooth muscle plasticity is also relevant in the context of vascular calibre and remodelling, where structural adaptations in the amount and organisation of contractile smooth muscle cells influence vascular constriction and tension generation. Furthermore, plasticity in airway smooth muscle may contribute to the development of chronic obstructive pulmonary diseases, airway hyper-responsiveness, and asthma. Smooth muscle plasticity is a dynamic and evolving area of research, with ongoing investigations into its role in disease progression and potential therapeutic interventions.
| Characteristics | Values |
|---|---|
| Smooth muscle plasticity | Smooth muscle cells can de-differentiate and become fibroblasts, thus becoming secretory in nature |
| Smooth muscle plasticity in atherosclerosis | Phenotypic modulation of smooth muscle cells in atherosclerosis is associated with downregulation of LMOD1, SYNPO2, PDLIM7, PLN, and SYNM |
| SMC plasticity in the context of vascular remodelling | SMC plasticity is more extensively studied on other hollow structures such as airway and bladder |
| SMC plasticity and inflammation | An increasing body of data suggests that SMC plasticity and the ability to perform nonprofessional phagocytic functions are key in cell-to-cell crosstalk with endothelial cells and immune cells during the complex process of inflammation |
| SMC plasticity and mechanical load | SMC plasticity may be a major factor in the development of pathophysiological conditions like chronic obstructive pulmonary diseases, airway hyper-responsiveness, and asthma |
| SMC plasticity and length-tension relationship | If we stretch smooth muscle, we see a small, temporary increase in passive tension, but that rapidly returns to normal. The ability of the smooth muscle cell to generate active tension remains normal over a very wide range of changes in length |
| SMC plasticity and force | SMCs reorganize their components to optimize the overlap between actin and myosin filaments to generate maximum force at the imminent length, maintaining functionality at a large range of distensions |
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What You'll Learn
Smooth muscle plasticity's role in atherosclerosis
Smooth muscle plasticity plays a significant role in atherosclerosis, a disease that remains the most prevalent cause of premature mortality worldwide. Atherosclerosis is a lipid-driven disease characterised by heightened inflammation, and vascular smooth muscle cells (VSMCs) have been found to play a causal role in this process.
Vascular smooth muscle cells are highly plastic, able to adapt their structure and function in response to their biomechanical environment. This plasticity is integral to the remodelling of blood vessels, allowing them to maintain functionality over a large range of distensions. Smooth muscle cells can dynamically reorganise their components, optimising the overlap between actin and myosin filaments to generate the maximum force at a given length. This contractile plasticity is well-studied in airway smooth muscle cells and has been implicated in the development of pathologies such as asthma.
In the context of atherosclerosis, VSMC plasticity contributes to the formation of atherosclerotic plaques. Lineage-tracing studies have confirmed that atherosclerotic lesions are composed of at least 30% VSMC-derived cells. The phenotypic modulation of VSMCs, characterised by reduced expression of contractile proteins, is associated with specific gene downregulation. This plasticity allows VSMCs to contribute to the fibrous cap, stabilising atherosclerotic plaques. However, VSMCs can lose their properties to the extent that they become challenging to identify, significantly contributing to the foam cell population and acquiring inflammatory-like cell features.
The diverse array of cell phenotypes derived from VSMCs within atherosclerotic plaques has been increasingly recognised for its beneficial and detrimental roles in plaque stability and disease burden. Recent findings have shed light on the underestimated deleterious role of VSMCs in atherosclerosis, highlighting the need to develop innovative new therapies to minimise atherosclerosis-related deaths further.
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Plasticity in airway smooth muscle
Smooth muscle is a type of muscle that differs from striated muscle in that it is plastic and adapts to changes in length. Smooth muscle cells have a large functional range and can adapt to changes in length by forming variable numbers of contractile units in series. This is known as plasticity, which is the ability to undergo physical changes or rearrangements.
The primary stimulus for plasticity in ASM is the level and dynamic character of the mechanical load posed upon the smooth muscle cells (SMCs). SMCs reorganize their components to optimize the overlap between actin and myosin filaments to generate maximum force at the imminent length, maintaining functionality at a large range of distensions. This is known as contractile plasticity. ASM has dynamic active and passive length-tension (L-T) curves, and the force generated by a smooth muscle bundle depends on the number of activated cross-bridges.
Mechanisms of mechanical plasticity in ASM include the polymerization and elongation of thin smooth muscle α-actin-containing filaments following the activation and clustering of β1 integrin focal adhesions. Another mechanism is the perturbed equilibrium model of myosin binding, where oscillatory strain on ASM during breathing is transmitted to the myosin head, causing unending perturbations of optimal actin and myosin binding. This results in the contractile machinery being kept off-balance and unable to achieve its full force-generating potential.
Studies on canine airway smooth muscle have examined the muscle length dependence of shortening velocity and compliance, which vary with the number of thick filaments in series. Temporary force depression after a length change is explained by the reforming of the filament lattice to produce optimum force development, with commensurate changes in velocity and compliance.
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Smooth muscle's response to stretch
Smooth muscle is one of the three major types of vertebrate muscle tissue and is found in the walls of hollow organs, including the stomach, intestines, bladder, and uterus. It is also present in the tracts of the respiratory, urinary, and reproductive systems, as well as in the eyes and skin. Smooth muscle-containing tissue needs to be stretched often, making elasticity an important attribute. This muscle is controlled by the autonomic nervous system and exhibits plasticity in response to stretch.
Smooth muscle cells undergo substantial increases in length, passively stretching during increases in intraluminal pressure in vessels and hollow organs. This passive tension evokes contraction, and one process by which this occurs is through the opening of mechano or stretch-sensitive ion channels. Stretch-induced calcium release (SICR) is observed in smooth muscle tissues, where longitudinal stretch induces Ca2+ release through ryanodine receptor gating. This release may be an important component of the physiological response to increases in luminal pressure.
The primary stimulus for contractile plasticity in smooth muscle is the level and dynamic character of the mechanical load. Smooth muscle cells reorganize their components to optimize the overlap between actin and myosin filaments to generate maximum force at a given length, maintaining functionality over a large range of distensions. This dynamic equilibrium of actin and myosin filaments underlies SMC plasticity.
Mechanical stretching of vascular smooth muscle cells has been shown to stimulate cell growth, nuclear protein import, and nuclear pore expression through mitogen-activated protein kinase (MAPK) activation. This process involves the MAPK pathway, which mediates the adaptation of nuclear protein import and nuclear pore density in response to mechanical stimuli during cell growth. The growth of vascular smooth muscle cells is an active process that requires the induction of cell cycle regulatory proteins.
In summary, smooth muscle exhibits plasticity in response to stretch by reorganizing its contractile units, optimizing the overlap of actin and myosin filaments, and stimulating cell growth through MAPK-mediated mechanisms. This plasticity allows smooth muscle to adapt to changes in length and mechanical load while maintaining functionality.
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SMC phenotypic modulation
Smooth muscle cells (SMCs) modulate their phenotype between proliferative and differentiated states in response to physiological and pathological cues. SMC phenotypic modulation is a dynamic process that involves the interaction of various cellular and molecular mechanisms.
One key mechanism of SMC phenotypic modulation is the regulation of gene expression. For example, the transcription factor Foxo4 interacts with myocardin, a transcriptional coactivator of smooth muscle genes. Foxo4 represses SMC differentiation by inhibiting myocardin's activity. Insulin-like growth factor-I stimulates SMC differentiation by activating the PI3K-Akt signaling pathway, which in turn promotes the nuclear export of Foxo4 and enhances myocardin activity.
Epigenetic regulation also plays a crucial role in SMC phenotypic modulation. Studies have shown that chromatin dynamics, histone modifications, and microRNA regulation influence SMC plasticity and phenotype. For instance, the binding of KLF4, pELK-1, and HDAC2 to a specific repressor element mediates transcriptional silencing during SMC phenotypic switching. Ten-eleven translocation-2 (TET2) is identified as a master regulator of SMC plasticity.
Additionally, SMC phenotypic modulation is associated with the expression of specific markers and the downregulation of certain genes. In atherosclerosis, SMC phenotypic modulation is linked to the downregulation of LMOD1, SYNPO2, PDLIM7, PLN, and SYNM. SMCs within atherosclerotic lesions can undergo phenotypic transitions and give rise to various cell types, including SMC-derived fibrous cap cells, macrophage-like cells, and mesenchymal-stem cell-like cells.
Furthermore, SMC plasticity is particularly relevant in the context of vascular remodelling and the development of pathophysiological conditions. SMCs reorganize their components, such as actin and myosin filaments, to optimize force generation and maintain functionality across a wide range of distensions. This contractile plasticity may contribute to the pathogenesis of diseases like chronic obstructive pulmonary disease, airway hyper-responsiveness, and asthma.
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SMC contractile plasticity
Smooth muscle cells (SMCs) are the primary cell type in the pre-atherosclerotic intima, a state known as diffuse intimal thickening (DIT). SMCs are not terminally differentiated and can change their phenotype in response to environmental cues, including growth factors/inhibitors, mechanical influences, cell-cell and cell-matrix interactions, extracellular lipids and lipoproteins, and various inflammatory mediators in the injured artery wall.
SMCs are organised such that maximum contractile force generally occurs at diameters slightly below the diameter at full dilation and physiological pressure. SMCs can thus undergo structural adaptation in response to changes in cell length, mechanical load, and contraction. SMCs reorganise their components to optimise the overlap between actin and myosin filaments to generate maximum force at the imminent length, maintaining functionality at a large range of distensions.
The primary stimulus for SMC contractile plasticity is the level and dynamic character of the mechanical load posed upon the SMCs. SMC plasticity is regulated by a complex network consisting of circulating plasma substances, transcription factors, growth factors, inflammatory factors, non-coding RNAs, integrin family, and Notch pathways.
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Frequently asked questions
Plasticity is used to describe long-term changes in how a cell or tissue functions. It may also refer to long-term changes in the appearance of the cell or tissue.
Smooth muscle plasticity refers to the ability of smooth muscle cells to change the mechanics of how they work, even though the basic mechanism of contraction remains the same. Smooth muscle plasticity is believed to be important in the development of atherosclerosis and primary pulmonary hypertension.
Smooth muscle plasticity is driven by the dynamic equilibrium of myosin and actin filaments. Myosin filaments slide over actin filaments in opposite directions during cross-bridge cycling, which generates mechanical force. Smooth muscles can also migrate over some distance, unlike skeletal muscles.
Smooth muscle plasticity plays a key role in cell-to-cell crosstalk with endothelial cells and immune cells during inflammation. It is also associated with vascular occlusive diseases and the development of pathophysiological conditions like chronic obstructive pulmonary diseases, airway hyper-responsiveness, and asthma. Smooth muscle plasticity is also linked to atherosclerosis and SMC phenotypic switching.
