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CALCIUM SPARKS AND CALCIUM SIGNALING IN HEART
钙火花研究进展与瞻望

ZHAO Ting,WEI Sheng,FANG Hua-qiang,WANG Xian-hua,ZHENG Ming,CHENG He-ping,
赵婷
,魏盛,方华强,王显花,郑铭,程和平

生物物理学报 , 2007,
Abstract: The calcium ion (Ca2+) is the simplest and the most versatile intracellular second messenger known to date. Over last decade, the discovery of Ca2+ sparks and a family of local elementary Ca2+ signaling events has unveiled a “digital-analog” feature of intracellular Ca2+ signaling. Brief, local “digital” Ca2+ microdomains and nanodomains are commingled with the continuous global “analog” Ca2+ signals. Patterned activation of digital Ca2+ signals confers on intracellular Ca2+ signaling a multi-scaled architecture in space, time and magnitude, and is of particular relevance in spatiotemporal regulation of high-threshold Ca2+-dependent processes (e.g., striated muscle excitation-contraction coupling, exocytosis). Investigation on spark activation, coordination, and termination has revealed new insights as well as perplexing questions about gating of Ca2+ release channels (ryanodine receptor, inositol 1,4,5-trisphosphate receptor) in intact cells, and brought about mechanistic understanding of the diverse and even opposing roles of Ca2+ signaling. Future investigation on “digital-analog” dichotomy of Ca2+ signaling thus holds the promise to unify the simplicity and complexity of Ca2+ signaling in biology.
The Role of Alpha-Dystrobrevin in Striated Muscle  [PDF]
Masayuki Nakamori,Masanori P. Takahashi
International Journal of Molecular Sciences , 2011, DOI: 10.3390/ijms12031660
Abstract: Muscular dystrophies are a group of diseases that primarily affect striated muscle and are characterized by the progressive loss of muscle strength and integrity. Major forms of muscular dystrophies are caused by the abnormalities of the dystrophin glycoprotein complex (DGC) that plays crucial roles as a structural unit and scaffolds for signaling molecules at the sarcolemma. α-Dystrobrevin is a component of the DGC and directly associates with dystrophin. α-Dystrobrevin also binds to intermediate filaments as well as syntrophin, a modular adaptor protein thought to be involved in signaling. Although no muscular dystrophy has been associated within mutations of the α-dystrobrevin gene, emerging findings suggest potential significance of α-dystrobrevin in striated muscle. This review addresses the functional role of α-dystrobrevin in muscle as well as its possible implication for muscular dystrophy.
Striated Muscle Regulation of Isometric Tension by Multiple Equilibria  [PDF]
Henry G. Zot,Javier E. Hasbun,Nguyen Van Minh
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0008052
Abstract: Cooperative activation of striated muscle by calcium is based on the movement of tropomyosin described by the steric blocking theory of muscle contraction. Presently, the Hill model stands alone in reproducing both myosin binding data and a sigmoidal-shaped curve characteristic of calcium activation (Hill TL (1983) Two elementary models for the regulation of skeletal muscle contraction by calcium. Biophys J 44: 383–396.). However, the free myosin is assumed to be fixed by the muscle lattice and the cooperative mechanism is based on calcium-dependent interactions between nearest neighbor tropomyosin subunits, which has yet to be validated. As a result, no comprehensive model has been shown capable of fitting actual tension data from striated muscle. We show how variable free myosin is a selective advantage for activating the muscle and describe a mechanism by which a conformational change in tropomyosin propagates free myosin given constant total myosin. This mechanism requires actin, tropomyosin, and filamentous myosin but is independent of troponin. Hence, it will work equally well with striated, smooth and non-muscle contractile systems. Results of simulations with and without data are consistent with a strand of tropomyosin composed of ~20 subunits being moved by the concerted action of 3–5 myosin heads, which compares favorably with the predicted length of tropomyosin in the overlap region of thick and thin filaments. We demonstrate that our model fits both equilibrium myosin binding data and steady-state calcium-dependent tension data and show how both the steepness of the response and the sensitivity to calcium can be regulated by the actin-troponin interaction. The model simulates non-cooperative calcium binding both in the presence and absence of strong binding myosin as has been observed. Thus, a comprehensive model based on three well-described interactions with actin, namely, actin-troponin, actin-tropomyosin, and actin-myosin can explain the cooperative calcium activation of striated muscle.
Calcium sparks in the intact gerbil spiral modiolar artery
Gayathri Krishnamoorthy, Keil Regehr, Samantha Berge, Elias Q Scherer, Philine Wangemann
BMC Physiology , 2011, DOI: 10.1186/1472-6793-11-15
Abstract: Calcium sparks were recorded from smooth muscle cells of intact arteries loaded with fluo-4 AM. Calcium sparks occurred with a frequency of 2.6 Hz, a rise time of 17 ms and a time to half-decay of 20 ms. Ryanodine reduced spark frequency within 3 min from 2.6 to 0.6 Hz. Caffeine (1 mM) increased spark frequency from 2.3 to 3.3 Hz and prolonged rise and half-decay times from 17 to 19 ms and from 20 to 23 ms, respectively. Elevation of potassium (3.6 to 37.5 mM), presumably via depolarization, increased spark frequency from 2.4 to 3.2 Hz. Neither ryanodine nor depolarization changed rise or decay times.This is the first characterization of calcium sparks in smooth muscle cells of the spiral modiolar artery. The results suggest that calcium sparks may regulate the diameter of the spiral modiolar artery and cochlear blood flow.The gerbil spiral modiolar artery (SMA) originates via the anterior inferior cerebellar artery from the basilar artery and provides the blood supply to the cochlea. It has an outer diameter of ~60 μm and follows the eighth cranial nerve from the brain stem to the modiolus of the cochlea [1]. The SMA is an end-artery that feeds the capillary networks of the spiral ligament and the stria vascularis, which maintains the endocochlear potential essential for hearing [2]. This energy-intensive mechanism renders the cochlea vulnerable to ischemia, which is thought to be involved in the pathogenesis of hearing loss and tinnitus. Consequently, the mechanisms that regulate the diameter of the SMA and thereby cochlear blood flow are of great interest.Vascular tone is determined by the contractility of the smooth muscle cell, which is regulated by membrane-potential and Ca2+-dependent as well as independent mechanisms [3]. An important regulator of smooth muscle contractility is the ryanodine receptor (RyR) mediated "Ca2+ spark". Ca2+ sparks are the physical manifestation of coordinated openings of clustered RyRs causing a highly localized and transient incre
Ultrastructure of developing human muscle: the problem of multinucleation of striated muscle cells
Minguetti, Guilberto;Mair, W. G. P.;
Arquivos de Neuro-Psiquiatria , 1986, DOI: 10.1590/S0004-282X1986000100001
Abstract: the authors studied by electron microscopy the muscle of 27 human foetuses ranging from 9 weeks to 9 months development. it was possible to observe that disintegration of the plasma membranes of adjacent myoblasts and myotubes which share a common basement membrane tube appears to occur in longitudinally disposed cells of those categories. this may help to explain how further nuclei may be incorporated into well developed myotubes and how the striated muscle cells become multinucleated during embryonic myogenesis and regeneration in vivo.
Contractile Properties of Esophageal Striated Muscle: Comparison with Cardiac and Skeletal Muscles in Rats
Takahiko Shiina,Takeshi Shima,Kazuaki Masuda,Haruko Hirayama,Momoe Iwami,Tadashi Takewaki,Hirofumi Kuramoto,Yasutake Shimizu
Journal of Biomedicine and Biotechnology , 2010, DOI: 10.1155/2010/459789
Abstract: The external muscle layer of the mammalian esophagus consists of striated muscles. We investigated the contractile properties of esophageal striated muscle by comparison with those of skeletal and cardiac muscles. Electrical field stimulation with single pulses evoked twitch-like contractile responses in esophageal muscle, similar to those in skeletal muscle in duration and similar to those in cardiac muscle in amplitude. The contractions of esophageal muscle were not affected by an inhibitor of gap junctions. Contractile responses induced by high potassium or caffeine in esophageal muscle were analogous to those in skeletal muscle. High-frequency stimulation induced a transient summation of contractions followed by sustained contractions with amplitudes similar to those of twitch-like contractions, although a large summation was observed in skeletal muscle. The results demonstrate that esophageal muscle has properties similar but not identical to those of skeletal muscle and that some specific properties may be beneficial for esophageal peristalsis.
Esophageal striated muscle contractions in patients with Chagas' disease and idiopathic achalasia
Dantas, R.O.;Aprile, L.R.O.;Aben-Athar, C.G.;Miranda, A.L.M.;
Brazilian Journal of Medical and Biological Research , 2002, DOI: 10.1590/S0100-879X2002000600007
Abstract: chagas' disease causes degeneration and reduction of the number of intrinsic neurons of the esophageal myenteric plexus, with consequent absent or partial lower esophageal sphincter relaxation and loss of peristalsis in the esophageal body. the impairment of esophageal motility is seen mainly in the distal smooth muscle region. there is no study about esophageal striated muscle contractions in the disease. in 81 patients with heartburn (44 with esophagitis) taken as controls, 51 patients with chagas' disease (21 with esophageal dilatation) and 18 patients with idiopathic achalasia (11 with esophageal dilatation) we studied the amplitude, duration and area under the curve of esophageal proximal contractions. using the manometric method and a continuous perfusion system we measured the esophageal striated muscle contractions 2 to 3 cm below the upper esophageal sphincter after swallows of a 5-ml bolus of water. there was no significant difference in striated muscle contractions between patients with heartburn and esophagitis and patients with heartburn without esophagitis. there was also no significant difference between patients with heartburn younger or older than 50 years or between men and women or in esophageal striated muscle contractions between patients with heartburn and chagas' disease. the esophageal proximal amplitude of contractions was lower in patients with idiopathic achalasia than in patients with heartburn. in patients with chagas' disease there was no significant difference between patients with esophageal dilatation and patients with normal esophageal diameter. esophageal striated muscle contractions in patients with chagas' disease have the same amplitude and duration as seen in patients with heartburn. patients with idiopathic achalasia have a lower amplitude of contraction than patients with heartburn.
Esophageal striated muscle contractions in patients with Chagas' disease and idiopathic achalasia  [cached]
Dantas R.O.,Aprile L.R.O.,Aben-Athar C.G.,Miranda A.L.M.
Brazilian Journal of Medical and Biological Research , 2002,
Abstract: Chagas' disease causes degeneration and reduction of the number of intrinsic neurons of the esophageal myenteric plexus, with consequent absent or partial lower esophageal sphincter relaxation and loss of peristalsis in the esophageal body. The impairment of esophageal motility is seen mainly in the distal smooth muscle region. There is no study about esophageal striated muscle contractions in the disease. In 81 patients with heartburn (44 with esophagitis) taken as controls, 51 patients with Chagas' disease (21 with esophageal dilatation) and 18 patients with idiopathic achalasia (11 with esophageal dilatation) we studied the amplitude, duration and area under the curve of esophageal proximal contractions. Using the manometric method and a continuous perfusion system we measured the esophageal striated muscle contractions 2 to 3 cm below the upper esophageal sphincter after swallows of a 5-ml bolus of water. There was no significant difference in striated muscle contractions between patients with heartburn and esophagitis and patients with heartburn without esophagitis. There was also no significant difference between patients with heartburn younger or older than 50 years or between men and women or in esophageal striated muscle contractions between patients with heartburn and Chagas' disease. The esophageal proximal amplitude of contractions was lower in patients with idiopathic achalasia than in patients with heartburn. In patients with Chagas' disease there was no significant difference between patients with esophageal dilatation and patients with normal esophageal diameter. Esophageal striated muscle contractions in patients with Chagas' disease have the same amplitude and duration as seen in patients with heartburn. Patients with idiopathic achalasia have a lower amplitude of contraction than patients with heartburn.
Tropomodulin Capping of Actin Filaments in Striated Muscle Development and Physiology
David S. Gokhin,Velia M. Fowler
Journal of Biomedicine and Biotechnology , 2011, DOI: 10.1155/2011/103069
Abstract: Efficient striated muscle contraction requires precise assembly and regulation of diverse actin filament systems, most notably the sarcomeric thin filaments of the contractile apparatus. By capping the pointed ends of actin filaments, tropomodulins (Tmods) regulate actin filament assembly, lengths, and stability. Here, we explore the current understanding of the expression patterns, localizations, and functions of Tmods in both cardiac and skeletal muscle. We first describe the mechanisms by which Tmods regulate myofibril assembly and thin filament lengths, as well as the roles of closely related Tmod family variants, the leiomodins (Lmods), in these processes. We also discuss emerging functions for Tmods in the sarcoplasmic reticulum. This paper provides abundant evidence that Tmods are key structural regulators of striated muscle cytoarchitecture and physiology.
Direct Regulation of Striated Muscle Myosins by Nitric Oxide and Endogenous Nitrosothiols  [PDF]
Alicia M. Evangelista,Vijay S. Rao,Ashley R. Filo,Nadzeya V. Marozkina,Allan Doctor,David R. Jones,Benjamin Gaston,William H. Guilford
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0011209
Abstract: Nitric oxide (NO) has long been recognized to affect muscle contraction [1], both through activation of guanylyl cyclase and through modification of cysteines in proteins to yield S-nitrosothiols. While NO affects the contractile apparatus directly, the identities of the target myofibrillar proteins remain unknown. Here we report that nitrogen oxides directly regulate striated muscle myosins.
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