Role of Triad in Muscle Contraction
an.r., undeclared; LGMD-1C, muscular dystrophy of the limbs of type 1C; RMD, undulating muscle disease; FHC, familial hypertrophic cardiomyopathy; LQTS, long QT syndrome; ARCNM, autosomal recessive centronuclear myopathy; SR, sarcoplasmic reticulum; XLMTM, X-linked myotubular myopathy; XLCNM, X-linked centronuclear myopathy. The importance of T tubules lies not only in their concentration of L-type calcium channels, but also in their ability to synchronize the release of calcium in the cell. The rapid propagation of the action potential along the tubular network T activates almost simultaneously all L-type calcium channels. Since the T tubules bring the sarcolemma to all regions of the cell very close to the sarcoplasmic reticulum, calcium can then be released from the sarcoplasmic reticulum over the entire cell at the same time. This synchronization of calcium release allows muscle cells to contract more tightly. [14] In cells without T tubules, such as smooth muscle cells, diseased cardiomyocytes or muscle cells in which the T tubules have been artificially eliminated, calcium entering the sarcolemma must gradually diffuse throughout the cell and activate ryanodine receptors much more slowly than a calcium wave, resulting in a less severe contraction. [14] Flucher BE, Takekura H, Franzini-Armstrong C: Development of the excitation-contraction coupling apparatus in skeletal muscle: association of the sarcoplasmic reticulum and transverse tubulis with myofibrils. Dev Biol. 1993, 160: 135-147. 10.1006/dbio.1993.1292.
Organization of the triad in skeletal muscles. Left: Electronic microscopic image of a triad transition. A central T tubule is flanked on both sides by a terminal cisternae element of the sarcoplasmic reticulum. The arrows indicate electron-dense connecting feet corresponding to the ryanodine receptor-dihydhropyridine receptor complex. Right: Schematic representation of mammalian muscular sarcoma and surrounding membranes. The T-tubules depicted in grey are specialized footprints of the sarcolemma. The elaborate network of sarcoplasmic reticulum is represented in blue. Note the proximity of the T-tubules and terminal cisternes of the sarcoplasmic reticulum (adapted by [104]; ©2007 by Pearson Education, Inc.).
The contraction of mature skeletal muscles is very resistant in conditions without Ca2+, and it is difficult to deplete SR as ca2+ intracellular memory. However, high resistance is not fully established in the immature muscles of neonatal mice. We examined the JP-1 knockout muscle in conditions without Ca2+ (Fig. 7 B). The mutated muscle showed a faster decrease in contraction tension than the control muscle. The apparent time constants of wild type muscle disintegration and JP-1 knockout were 13.7 and 7.4 min, respectively. A similar result was observed in the Mitsugumin29 knockout muscle, which carries structurally irregular membrane systems around the triad transition (Nishi et al., 1999). Observations on mutated muscles without Mitsugumin29 or JP-1 suggest that the formation of refined triad compounds is important for the mechanism of ca2+ maintenance in skeletal muscles. Komazaki S, Nishi M, Kangawa K, Takeshima H: Immunolocation of mitsugumin29 in skeletal muscle development and effects of protein expressed in amphibious embryonic cells.
Dev Dyn. 1999, 215: 87-95. 10.1002/(SICI)1097-0177(199906)215:23.0.CO;2-Y. Takekura H, Flucher BE, Franzini-Armstrong C: Sequential docking, molecular differentiation and positioning of T-Tubule/SR junctions in mouse skeletal muscle development. Dev Biol. 2001, 239: 204-214. 10.1006/dbio.2001.0437. The structure of the T-tubules can be altered by diseases that can contribute to weakness of the heart muscle or cardiac arrhythmias in the heart. The changes observed in diseases range from a complete loss of T tubules to more subtle changes in their orientation or branching patterns. [29] T tubules can be lost or disturbed after a myocardial infarction[29], and are also disturbed in the ventricles of patients with heart failure, contributing to a decrease in contractility and possibly reducing the chances of recovery. [30] Heart failure can also lead to the almost complete loss of the T tubules of atrial cardiomyocytes, reducing atrial contractility and potentially contributing to atrial fibrillation. [27] Expression of JP subtypes in skeletal muscle.
(A) Western blot analysis of JP subtypes in mouse tissues. The total microsomes of adult mouse tissue (15 μg protein each) were analyzed with specific antibodies jp-1 and JP-2. B, brain; H, heart; K, kidney; L, liver; SM, skeletal muscles. Size markers are displayed in kilodaltons. JP-2 has been shown to be a wide band in skeletal muscle due to comigration with Ca2+-ATPase, the main protein component of SR. (B) Western transfer analysis of JP subtypes during muscle maturation. Overall, hind leg microsomes (40 μg protein each) produced between embryonic mice on day 14 (E14) and postnatal day 28 (P28) were analyzed with subtype-specific antibodies. Although JP-1 expression in embryos and newborns could be demonstrated with prolonged exposure (see Fig. 2), signal densities were significantly lower than in young adult mice.
Unlike JP-1, the induction of JP-2 expression during muscle maturation was relatively loose. (C) Immunohistochemical analysis of jp subtypes in skeletal muscle. Cryosection of the hind leg muscle of adult mice was immunofluorescence using antibodies specific to JP-1 (at an excitation of 543 nm) and JP-2 (at an excitation of 488 nm). The immune-labelled cytoplasmic series with both antibodies are localized to identical (fused) positions. Essentially, the same patterns of staining were observed in all muscle fibers studied in the hind leg muscle. Bar, 10 μm. Since JP-1 is mainly expressed in skeletal muscle, we studied morphological defects in skeletal muscle in newborn KO JP-1. The cell density, diameter and shape of the mutated muscle fibers appeared to be normal, and photomicroscopic examination revealed no obvious abnormalities.
However, electron microscopic examination revealed ultrastructural abnormalities in the membrane systems of the mutated muscles (Fig. 4). In the muscles of newborn mice, the formation of connection complexes between the tubule T and the SR is not yet complete, and diades and triads partially occupy the A-I compounds. Unlike flattened T-tube structures in mature triads, the T-tubules pinched by the SR on both sides in the immature muscles of newborns are often elliptical. No obvious ultrastructural abnormalities in the membrane system were observed in the mutated muscles of KO JP-1 newborns immediately after birth. However, the mutated muscles of knockout newborns about to die (15 to 20 h after birth) showed the following abnormal characteristics: the terminal regions of the SR were often swollen, the longitudinal regions of SR were partially vacuolated, and the alignment of the SR networks was irregular. Therefore, the connecting membrane complexes of the diades and triads in the mutated muscles were structurally abnormal. These morphological abnormalities were detected in all types of muscles examined in newborns 15 to 20 hours after birth, and the muscle cells of the jaw showed the most serious defects.
On the other hand, mitochondria and myofibrils maintained normal structures in the JP-1 knockout muscles. Quantitative analysis of the junctional membrane structures between wild skeletal muscles and JP-1 knockout. Skeletal muscles were made from the tongue, jaw (digastile), diaphragm and buttocks (thigh area) of newborn mice immediately after birth. The junctional membrane structures of the A-I compounds were analyzed by electron microscopic observations and the results of random samples between genotypes were compared. The data come from at least 3,000 A-I compounds from three newborns and are presented as an average ± REM. Statistical differences between genotypes are indicated by asterisks (t-test, *P < 0.05 and **P < 0.01). Treatment of isolated muscle fibers with an influx of glycerin efflux or with other low-muscle non-electrolytes (such as sugars) has been reported to physically affect the morphology of the T tubules. Such osmotic shock can convert the T-tubule network into many membrane-bound vacuoles that remain connected by normal T tubules or can be separated (Figure 2) [9, 10]. Surprisingly, this vacuolation, which leads to a 5 to 15-fold increase in the relative volume of the tubular T-shaped system, is spontaneously reversed [11, 12]. Moreover, this observation is specific to transverse tubular membranes, as no other intracellular membrane system appears to be involved [12], probably due to the fact that their light is connected to the extracellular space.
T-tubules are an important link in the chain from the electrical excitation of a cell to its subsequent contraction (excitation-contraction coupling). When a muscle contraction is required, stimulation by an adjacent nerve or muscle cell causes a characteristic flow of charged particles across the cell membrane called the action potential. .
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