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Kamkin A, Kiseleva I, editors. Mechanosensitivity in Cells and Tissues. Moscow: Academia; 2005.

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Mechanosensitivity in Cells and Tissues.

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Mechanosensitivity of Cells from Various Tissues

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Department of Fundamental and Applied Physiology, Russian State Medical University, Ostrovitjanova Str. 1, 117997 Moscow, Russia
*Corresponding author: Andre Kamkin, M.D., Ph.D., Dr.med.habil. Department of Fundamental and Applied Physiology. Russian State Medical University. Ostrovitjanova Str. 1, 117997 Moscow, Russia, Phone: 007095-131 4863, Telefax: 007095-131 4863, e-mail: ur.mocler.32g@A.nikmaK

Mechanosensitivity, i.e. the specific response to mechanical stimulation, is common to a wide variety of cells in many different organisms ranging from bacteria to mammals. Mechanical stress can modulate physiological processes at the molecular, cellular, and systemic level. The primary target for mechanical stimulation is the plasma membrane of the cell, which can respond to variable physical stress with changes of the open probability of mechanosensitive ion channels. Thus, acting on ion channels in the plasma membrane, mechanical stress can elicit a multitude of biochemical processes – both transient and long-lasting – inside a cell. This may ultimately influence the function of tissues and organs in health and disease. Several stretch-induced signaling cascades have been described with multiple levels of crosstalk between the different pathways. Increased sensitivity of the cells to mechanical stress is found under various pathological conditions. A detailed study of the underlying mechanisms may therefore help to identify novel therapeutic targets for a future clinical use.

Introduction

In the evolution process, mechanical stress is most ancient irritant. Response to mechanical stress is characteristic for organisms at various stages of evolutionary development, from bacteria to mammals. Thus, mechanosensitivity is a universal quality found in most types of cells. Mechanical stress starts electrophysiological and biochemical responses in cells. Mechanical stress can influence physiological processes at the molecular, cellular, and systemic level.

The primary target for mechanical stimulation is the plasma membrane of the cell, which can respond to variable physical stress with changes of the open probability of mechanosensitive ion channels (MSC). These channels include, e.g. stretch-activated channels – SAC (see for review [3, 44, 107, 160]), stretch-inactivated channels – SIC (see for review [18, 44, 107, 135]), pressure-activated channels – PAC (see for review [82, 83, 84, 106]). Besides the channels described above, there are stretch-activated K+-channels – SACK, that can be Ca2+ sensitive [42, 76, 132, 137] or Ca2+ insensitive [78, 124]. A particular position belongs to suction and swelling-activated chloride channels [4, 5, 6, 139, 140].

MSC can produce considerable currents in cells and play an important role in forming their electric response. Moreover, various membrane deformation can include different MSC types and this results in different electrophysiological cell responses [64]. At the same time, it is not clear yet how mechanical energy is transferred to MSC: through the lipid bilayer of the membrane or through the cytoskeleton and which of the mechanisms prevails [131]. It is possible that both mechanisms of transferring mechanical energy to MSC take place. It is also unclear how the MSC activities are regulated. A certain amount of MSC was cloned [144] and those works are a promising trend in studying this type of channels. There are studies of genes coding mechanosensitive system in nematodes [51, 63, 152]. Ongoing is the search for specific blockers for MSC [10, 123, 143].

It is relatively long ago that the concept of mechanoelectrical feedback was formulated [75, 87] and then it has been proved experimentally in numerous investigations (see for example [33, 34, 35, 46, 48, 49, 53, 54, 55, 61, 62, 88, 89, 90, 91, 92, 93, 94, 95, 116, 117, 118, 119, 120]). Originally, this concept considered electrical response to cell deformation. Nowadays, this problem is approached on a much broader basis, which allowed to form the concept of crosstalk in mechanotransduction. Mechanical stress can cause a number of short or long-lasting biochemical processes inside a cell. This can result in affecting the functions of healthy or diseased tissues and organs. Several stretch-induced signaling cascades have been described with multiple levels of crosstalk between the different pathways. Under various pathological conditions, mechanical stress causes increased cell sensitivity. A thorough research of the underlying mechanisms will be a big step forward in identifying novel therapeutic targets for a future clinical use.

Investigation of the molecular mechanisms of mechanotransduction

Genetic and molecular data obtained from the studies of model organisms such as the bacterium Escherichia coli, the nematode worm Caenorhabditis elegans, the fruit fly Drosophila melanogaster, and the mouse help to distinguish between classes of mechanically gated ion channels and interacting molecules, which are likely parts of the mechanotransducing apparatus.

Among prokaryotic MSC studied to date, the best characterized are the MSC of the bacterium Escherichia coli [108]. Three types of MSC were identified in E. coli, which based on their conductance were named as MscM (M for mini), MscS (S for small) and MscL (L for large) [8]. Bacterial MSC were the first shown to sense directly membrane tension in the lipid bilayer caused by external mechanical force applied to a cell membrane [105]. MscL is non-selective, MscS was more selective for anions over cations [106], MscM was reported to exhibit a slight preference for cations over anions [8, 9]. The activity of MscL and MscM is not dependent on voltage. MscS displays voltage dependence [106].

Caenorhabditis elegans possesses behavioral withdrawal responses to touch that have been used to isolate a number of touch insensitive mutants [60, 63]. Mechanotransduction in the nematode C. elegans was discussed in many studies (e.g., [38, 56, 145, 147, 148, 149, 150, 151, 152]). In the review by Voglis and Tavernarakis [153], presented in this book, they discuss models for mechanotransduction in C. elegans neurons, which implements genetic data and molecular properties of cloned genes. This model also based on mutant phenotypes, cell morphology, heterologous degenerin expression approaches, and structural features of degenerins remains to be tested by determining sub-cellular channel localization, subunit associations and, most importantly, channel gating properties. Under discussion is the scheme of the mechanotransducing complex in C. elegans touch receptor neurons. In the absence of mechanical stimulation, the channel is closed and therefore the sensory neuron is idle. Application of a mechanical force to the body of the animal results in distortion of a network of interacting molecules that opens the degenerin channel. Na+ influx depolarizes the neuron initiating the preceptory integration of the stimulus.

Drosophila is known to have MSCs in striated muscle [162], and mechanosensitive mutants have been constructed that exhibit a block of the behavioral response and the mechanosensitive field potentials of the antennae [77]. The recent identification of another strong candidate for a mechanosensory channel, the Drosophila NompC, adds to the list of candidate mechanosensitive ion channels [158].

Mechanosensitivity in the heart

The heart is sensitive to mechanical deformation. Characteristically, the beat rate increases with atrial pressure. Bainbridge was the first who recognized that acute distension of the right atrium by increased venous return caused the acceleration of heart rates [2]. He reasoned that locally acting mechanical forces could modulate the frequency of spontaneous myocardial contractions.

The response of the heart to mechanical pressure manifesting itself in changed electrical qualities of cardiomyocytes was postulated by M. J. Lab [87, 91, 94, 98] as a concept of mechanoelectric feedback in the heart. This concept was studied by various methods including ECG (e.g., [36]), registration of monophase potentials (e.g., [47, 49, 52, 115]), registration of intracellular potentials by microelectrodes [73, 80], registration of whole-cell currents [67, 68, 72, 163, 164], and single-channels recording (e.g., [121, 164]). It has been postulated that many of the fatal arrhythmias that follow a heart attack are caused by stretch of the weak tissue around the infarct which then generates excitatory currents [54]. SACs have been reported in heart cells from rat [28, 29, 164], chick [130], and snail [137]. Other issues of mechanosensitivity were investigated, such as whether stretch-induced changes in intracellular calcium modify the electrical activity of cardiac muscle [14]. Furthermore, it was shown that nitric oxide regulates cardiac contractility and stretch responses [17] and it is important messenger in the mediation of cardiac stretch responses [128]. Already a first SAC-specific blocker was identified [143]. It was demonstrated that in the heart the mechanosensitivity is present also in the connective tissue – the cardiac fibroblasts [69].

The major achievements of recent years in the field of studying mechanosesitivity in the heart are presented in this book as a review [7, 15, 20, 41, 65, 71, 74, 97, 129, 155, 161].

At present, the problem of mechanoelectrical feedback is interpreted more broadly and a concept of crosstalk of pathways of stretch-induced signaling cascades into the cell is suggested [96, 99]. The formed crosstalk concept [97], is based on the earlier researches on the issue [96, 99] and discusses possible signaling cascades in detail.

The forces that act on cell membranes can either be in form of direct mechanical deformation or as osmotic changes leading to cell swelling or shrinkage.

At the moment, one of the most important trends of research is the problem of volume-activated channels that are not well investigated yet, but can be of significance for normal or pathological state in changed intracellular osmolarity. Among the volume-activated channels, the outwardly rectifying, swelling-activated Cl- channels have been investigated most carefully [5, 6, 11, 12, 22, 23, 24, 25, 26, 27]. Multiple stimuli activate swelling-activated Cl- current. These channels react not only to the changed volume of the cell but also to the changed pressure in the patch-pipette. Of particular interest is the regulation of swelling-activated Cl- current by signaling cascades [7]. The release of autocrine and paracrine factors (i.e. angiotensin II and endothelin), which act on cardiomyocytes through angiotensin II signaling cascade seems to be of high importance [7]. Besides cardiac fibroblasts, the source of these factors can be the cardiomyocytes themselves [133].

In recent years, the problem of direct axial stretch of isolated cardiomyocytes from adult animals and humans was solved and studies have been performed characterizing whole-cell currents under artificial axial stretch or squeeze. In general, it was believed that direct stretching of isolated cardiomyocytes would cause huge problems [131]. A breakthrough was published in 2000 were the successful stretching of atrial and ventricular cardiomyocytes was reported [66, 67, 163, 164].

Stretching of atrial cardiomyocytes allowed the investigation and discussion of stretch-activated whole-cell currents [161]. These authors were the first to describe mechanically induced potentials and currents in isolated cardiomyocytes from rat atria [164]. Studies of human isolated atrial cardiomyocytes described not only mechanosensitive currents, but also demonstrated an increased sensitivity to stretch in atrial cardiomyocytes from hypertrophied hearts [72].

Also the response to stretch of ventricular cardiomyocytes was studied not only in cells of healthy animals, but also in cells from animals and humans with cardiac hypertrophy [67, 68]. Presently, the electrophysiological responses to a homogenous axial stretch of cardiomyocytes and their relation to changes in Na+ and Ca2+ concentration in the cytosol and in the cell organelles are discussed [65]. In recent years, a good correlation between the results from experiments carried out as whole-cell recordings from isolated cardiomyocytes and the results obtained from microelectrode recordings in stretched fragments of atria and ventricles from healthy animals and humans and those with hypertrophied myocardium has been recognized [74]. Before, it was believed that the latter task was practically not feasible [131]. But like with cardiomyocyte stretching by a glass stylus [66, 67], the technical problem of keeping a floating microelectrode in the tissue for a considerably long time, has been solved [73, 80].

The most important finding of these experiments was the discovery of a highly increased sensitivity to stretch in cells from hypertrophied myocardium. This increased sensitivity to stretch could be explained by altered signaling pathways or increased channel expression in hypertrophied myocardium. These data particularly allow to explain the origin mechanisms of mechanically-induced arrhythmias. Besides, it was shown that reactions to stretch or compression are different and the response to compression was different in the same cell determined by its spatial position [74].

Fundamentally new aspects in studying mechanosensitivity of heart cells are devoted to mechanosensitivity of cardiac fibroblasts, their intercellular interaction with each other and with cardiomyocytes [71]. Electrophysiological characteristics of cardiac fibroblasts and their intercellular relations were first described back in 1978 [70, 81]. At present, it has been proved that cardiac fibroblasts act as mechano-electrical transducers in the heart and they can participate in regulating the electrical activities of both, healthy and hypertrophied hearts [69].

A number of new research deals with mechanical modulation. Based on the Starling effect [45, 125, 141] immediate force response is discussed and a slow force response – based on the Anrep effect [154]. It has since been established that the mechanism for the slow response is intrinsic to cardiac muscle. Under discussion are the ways of transferring mechanical signals in these conditions.

At present, studies concentrate on changes that occur at the cellular level during the biphasic response to stretch, with particular reference to the modulation of intracellular concentrations of Na+ and Ca2+. Discussed is a secondary slow response [15]. Changes in intracellular Na+ and Ca2+ have implications not only for contractility, but also for the activity of ion channels and exchangers that are sensitive to these ions. Under discussion are the consequences that stretch-induced changes in intracellular Na+ and Ca2+ have for the electrical activity of the heart.

Other authors study a slow force response to stress, thus complementing one another [20, 155]. Slow force response is connected to stretch-induced Ca2+ transients under conditions of changed haemodynamics, or other ways, e.g. a stretch-induced autocrine/paracrine cascade that is related to release of angiotensin II and endothelin-1 with consecutive stimulation of the Na+/H+ exchanger resulting in enhanced transsarcolemmal Na+ entry. This is followed by a [Na+]i-dependent Ca2+ entry via the Na+/Ca2+ exchanger working in its reverse mode [1, 21, 127]. Furthermore a number of authors describe stretch-induced alterations in action potential duration, cAMP, or NO signaling [16, 156, 157]. These issues are discussed at different levels – whole heart, multicellular preparations, and isolated cardiomyocytes [20, 155]. Works under discussion give impetus to further research in the field of cardiac physiology and clinical cardiology [20, 155].

All the data presented allow to tackle the problem of arrhythmia originating mechanisms.

Atrial arrhythmia accompanies various heart diseases. A mechanical factor definitely participates in the development of atrial fibrillation. Atrial dilation often results in the development of atrial fibrillation. But the mechanism of fibrillation origins is not completely clear. The role of mechano-electrical feedback for arrhythmia was studied in atrial and ventricular myocardium. This problem remains an acute subject of research at present and this book presents two experimental models, one of which studied the impact of mechanical factor at the level of the whole heart under independently changed pressure in various cavities [129]. In this model, basic electrophysiological characteristics of atrial myocardium change dependent on pressure.

The other model considers the role of cholinenergic factors in the development of atrial fibrillation in vivo and demonstrates that an increased tone of the vagus nerves can play a role in developing atrial fibrillation [54].

Mechanosensitivity in the nervous system

Mechanosensitivity and mechanosensitive ion channels were studied by various methods in different structures of the nervous system from receptors to nerve cells [13, 19, 86, 104, 110, 111, 114, 135, 138, 142, 146]. The basic problem is how the surrounding mechanical factors affecting the membrane are transformed into various biochemical responses at the cellular level [102], that regulate the growth and differentiation of cells.

Mechanosensitive cation channels are discussed in leech nerve cells and their possible role in neurons is considered [126]. Leech neuron channels are similar to typical mechanosensitive cation channels of vertebrates' hair cells. Neuron membrane deformation in leech is a good model for studying crosstalk at the nerve cell level.

The problem of pain is important in clinical conditions but specific mechanisms involved in response to pain stimulus are not understood completely. There is need for further research of different responses of afferent and efferent neurons participating in the origins of pain perception. The present book discusses new results relating to mechanisms of pain. An important cell type connected with mechanosensitivity are the primary afferent nociceptors in the pain perception pathway [40]. The data under discussion allow a better understanding of visceral and somatic pains.

Mechanical factor can also modulate the activity of endocrine cells [136]. This review summarizes the basis for stimulus-secretion coupling and recent developments from the tilapia PRL cell model, in the light of other cell types and model systems.

Mechanosensitivity in skeletal muscle

Mechanosensitive channels of skeletal muscle are studied in detail [32, 43, 44, 50, 57, 85, 109, 159]. Of major interest is the research on mechano-sensitive ion channels in skeletal muscle from normal and dystrophic mice (see [43, 57]). The achievements of recent years are summarized in the book as review [101]. The review considers the mdx mouse, a deletion mutant that lacks full-length dystrophin, which has been used to investigate the role of the cytoskeleton in mechanosensitive channel gating [101].

Mechanosensitivity in smooth muscle

Smooth muscle from various preparations exhibit nonselective, K+-selective and Ca2+-selective mechanosensitive currents [37, 58, 59, 78, 79, 100, 122].

The book review [134] considers the MSC of smooth muscle and discusses their role in self-regulation of circulation and capillary hydrostatic pressure in various organs. Smooth muscles in small arteries and arterioles contribute greatly to autoregulation. Smooth muscles of the vessel walls contribute to the mechanism of autoregulation independently of endothelium and nerve influences and the autoregulation mechanism can change with diseases such as hypertension and diabetes. The review discusses transfer mechanisms at the cellular level. Additional details of this mechanism as well as the possible contributions of alternative pathways are the subjects of current investigations. Involvement of various channels is discussed [134].

Bone tissue, chondrocytes, and osteoblasts

Mechanical factors play an important role in forming bones and regeneration of osseous tissue. Mechanical factors regulate osteogenesis. Bone cells respond to mechanical impact but the process of transferring the mechanical stimulus is not clear yet. At the same time a lot of signal pathways have been shown able to take part in the process of mechanotransduction. Researching the impact of pressure on bone tissue is important not only for clinical conditions, but also for such conditions as prolonged weightlessness. There are a number of studies in regard to that respect.

Bone remodeling is the continuous turnover of bone matrix and mineral by bone resorption (activity of osteoclasts) and formation (activity of osteoblasts) in the adult skeleton, i.e. osteoblasts at the surface of the bone matrix are instrumental in synthesizing bone matrix proteins. Clonal UMR-106 cells derived from rat osteogenic sarcoma possess an 18 pS SA channel capable of conducting barium and calcium into the cell [39]. This channel is voltage insensitive, but its susceptibility to membrane tension suggests a role in volume regulation or as a stimulus for bone metabolism in response to mechanical stress. The finding of three types of SA channels in human osteoblast-like G292 osteosarcoma cells [30] lends weight to this suggestion. Mechanosensitive K(Ca) channels have also been reported in osteoblast cell lines [31].

Data from recent years describe signal transduction pathways and effects of mechanical strain in osteoblastic cells [103]. Mechanical strain plays a crucial role in bone growth, remodeling, and repair, where mechanosensing cells, most likely osteoblasts and osteocytes, direct these processes [103].

Studying the mechanosensitivity of chondrocytes, cells that respond to a wide variety of mechanical factors, is extremely important [113]. The role of mechanosensitive ion channels, β1-integrins and MAP kinase pathways in chondrocyte mechanotransduction is discussed. There is considerable evidence that ion channels residing in the plasma membrane of chondrocytes and osteoblasts are involved in the transduction of mechanical signals [113].

The enigmatic role of the epithelial sodium channel in articular chondrocytes and osteoblasts are considered and issues of mechanotransduction, sodium transport, or extracellular sodium sensing are discussed [112].

Conclusion and perspectives

In principle, the articles presented in this book prove that the issue of mechanoelectric feedback considering transformation of mechanical signals into electrical one has grown into a global field of investigating with special respect to the pathways activated by stretch. This very first edition does not include all the articles devoted to mechanosensitive tissues, but in the next edition, we plan to present more detailed reviews in varied fields of cell and tissue research.

Acknowledgement

This study was supported by the Alexander von Humboldt-Stiftung, a travel grant from the Humboldt University (Germany) and Russian State Medical University.

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