Excitation-Contraction Coupling in Fast- and Slow-Twitch Muscle Fibers

1987 ◽  
Vol 08 (06) ◽  
pp. 360-364 ◽  
Author(s):  
J. Rüegg
Keyword(s):  
Muscle Fibers ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Slow Twitch Muscle ◽  
Slow Twitch

scholarly journals T-tubule disorganization and defective excitation-contraction coupling in muscle fibers lacking myotubularin lipid phosphatase

2009 ◽  
Vol 106 (44) ◽  
pp. 18763-18768 ◽  
Author(s):  
L. Al-Qusairi ◽  
N. Weiss ◽  
A. Toussaint ◽  
C. Berbey ◽  
N. Messaddeq ◽  
...  
Keyword(s):  
Muscle Fibers ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Lipid Phosphatase

scholarly journals lncRNA-Six1 Is a Target of miR-1611 that Functions as a ceRNA to Regulate Six1 Protein Expression and Fiber Type Switching in Chicken Myogenesis

Cells ◽  
2018 ◽  
Vol 7 (12) ◽  
pp. 243 ◽  
Author(s):  
Manting Ma ◽  
Bolin Cai ◽  
Liang Jiang ◽  
Bahareldin Ali Abdalla ◽  
Zhenhui Li ◽  
...  
Keyword(s):  
Fiber Type ◽  
Muscle Fibers ◽  
Muscle Fiber Types ◽  
Fiber Types ◽  
Proliferation And Differentiation ◽  
Slow Twitch Muscle ◽  
Fast Twitch Muscle ◽  
Slow Twitch ◽  
Slow Twitch Fibers ◽  
Fast Twitch

Emerging studies indicate important roles for non-coding RNAs (ncRNAs) as essential regulators in myogenesis, but relatively less is known about their function. In our previous study, we found that lncRNA-Six1 can regulate Six1 in cis to participate in myogenesis. Here, we studied a microRNA (miRNA) that is specifically expressed in chickens (miR-1611). Interestingly, miR-1611 was found to contain potential binding sites for both lncRNA-Six1 and Six1, and it can interact with lncRNA-Six1 to regulate Six1 expression. Overexpression of miR-1611 represses the proliferation and differentiation of myoblasts. Moreover, miR-1611 is highly expressed in slow-twitch fibers, and it drives the transformation of fast-twitch muscle fibers to slow-twitch muscle fibers. Together, these data demonstrate that miR-1611 can mediate the regulation of Six1 by lncRNA-Six1, thereby affecting proliferation and differentiation of myoblasts and transformation of muscle fiber types.

Extracellular divalent cations in excitation–contraction coupling: hypertonic solution effects

1982 ◽  
Vol 60 (4) ◽  
pp. 440-445
Author(s):  
Isao Oota ◽  
Isao Kosaka ◽  
Torao Nagai ◽  
Hideyo Yabu
Keyword(s):  
Skeletal Muscle ◽  
Divalent Cations ◽  
Muscle Fibers ◽  
Hypertonic Solution ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Skeletal Muscle Fibers ◽  
Membrane Bound

It is the purpose of this article to point out that the membrane-bound Ca plays an important role in excitation–contraction (E–C) coupling of skeletal muscle fibers and that other divalent cations are unable to substitute for this role of membrane-bound Ca.

scholarly journals β3-Adrenergic agonist induces a functionally active uncoupling protein in fat and slow-twitch muscle fibers

1998 ◽  
Vol 274 (3) ◽  
pp. E469-E475 ◽  
Author(s):  
Toshihide Yoshida ◽  
Tsunekazu Umekawa ◽  
Kenzo Kumamoto ◽  
Naoki Sakane ◽  
Akinori Kogure ◽  
...  
Keyword(s):  
Uncoupling Protein ◽  
Muscle Fibers ◽  
Ectopic Expression ◽  
Brown Fat ◽  
Obese Mice ◽  
Adrenergic Agonist ◽  
Brown Adipose ◽  
Slow Twitch Muscle ◽  
Slow Twitch ◽  
White Fat

The mitochondrial uncoupling protein (UCP) has usually been found only in brown adipose tissue. We recently observed that a chronic administration of the β3-adrenergic agonist CL-316,243 (CL) induced the ectopic expression of UCP in white fat and skeletal muscle in genetic obese yellow KK mice. The aim of the present study was to examine whether UCP could be induced in nongenetic obese animals produced by neonatal injections of monosodiuml-glutamate (MSG). The daily subcutaneous injection of CL (0.1 mg/kg) to MSG-induced obese mice for 2 wk caused significant reductions of body weight (15%) and white fat pad weight (58%). Northern and Western blot analyses showed that CL induced significant expressions of UCP in the white fat and muscle, as well as in brown fat. Immunohistochemical observations revealed that the UCP stains in white fat were localized on multilocular cells and that those in muscle were localized on slow-twitch fibers rich in mitochondria. Immunoelectron microscopy confirmed the mitochondrial localization of UCP in the myocytes. The guanosine 5′-diphosphate (GDP) binding to mitochondria in brown fat doubled after the CL treatment. Moreover, significant GDP binding was detected in the white fat and muscle of the CL-treated mice, at about one-fourth and one-thirteenth the activity of brown fat, respectively, suggesting that ectopically expressed UCP is functionally active. We concluded that the β3-adrenergic agonist CL can induce functionally active UCP in white fat and slow-twitch muscle fibers of obese mice.

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