scholarly journals Simulation of Myoplasmic Calcium Transients in Mouse Slow-Twitch Muscle Fibers

2012 ◽  
Vol 102 (3) ◽  
pp. 366a
Author(s):  
Stephen M. Baylor ◽  
Stephen Hollingworth
Keyword(s):  
Muscle Fibers ◽  
Calcium Transients ◽  
Slow Twitch Muscle ◽  
Slow Twitch

scholarly journals Measurement of Myoplasmic Calcium Transients in Mouse Slow-Twitch Muscle Fibers

2012 ◽  
Vol 102 (3) ◽  
pp. 366a
Author(s):  
Stephen Hollingworth ◽  
Michele M. Kim ◽  
Stephen M. Baylor
Keyword(s):  
Muscle Fibers ◽  
Calcium Transients ◽  
Slow Twitch Muscle ◽  
Slow Twitch

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.

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.

scholarly journals Comparison of regulated passive membrane conductance in action potential–firing fast- and slow-twitch muscle

2009 ◽  
Vol 134 (4) ◽  
pp. 323-337 ◽  
Author(s):  
Thomas Holm Pedersen ◽  
William Alexander Macdonald ◽  
Frank Vincenzo de Paoli ◽  
Iman Singh Gurung ◽  
Ole Bækgaard Nielsen
Keyword(s):  
Action Potential ◽  
Muscle Fibers ◽  
Membrane Conductance ◽  
Fiber Types ◽  
Channel Inhibition ◽  
Slow Twitch Muscle ◽  
Slow Twitch ◽  
Slow Twitch Fibers ◽  
Fast Twitch ◽  
Passive Membrane

In several pathological and experimental conditions, the passive membrane conductance of muscle fibers (Gm) and their excitability are inversely related. Despite this capacity of Gm to determine muscle excitability, its regulation in active muscle fibers is largely unexplored. In this issue, our previous study (Pedersen et al. 2009. J. Gen. Physiol. doi:10.1085/jgp.200910291) established a technique with which biphasic regulation of Gm in action potential (AP)-firing fast-twitch fibers of rat extensor digitorum longus muscles was identified and characterized with temporal resolution of seconds. This showed that AP firing initially reduced Gm via ClC-1 channel inhibition but after ∼1,800 APs, Gm rose substantially, causing AP excitation failure. This late increase of Gm reflected activation of ClC-1 and KATP channels. The present study has explored regulation of Gm in AP-firing slow-twitch fibers of soleus muscle and compared it to Gm dynamics in fast-twitch fibers. It further explored aspects of the cellular signaling that conveyed regulation of Gm in AP-firing fibers. Thus, in both fiber types, AP firing first triggered protein kinase C (PKC)-dependent ClC-1 channel inhibition that reduced Gm by ∼50%. Experiments with dantrolene showed that AP-triggered SR Ca2+ release activated this PKC-mediated ClC-1 channel inhibition that was associated with reduced rheobase current and improved function of depolarized muscles, indicating that the reduced Gm enhanced muscle fiber excitability. In fast-twitch fibers, the late rise in Gm was accelerated by glucose-free conditions, whereas it was postponed when intermittent resting periods were introduced during AP firing. Remarkably, elevation of Gm was never encountered in AP-firing slow-twitch fibers, even after 15,000 APs. These observations implicate metabolic depression in the elevation of Gm in AP-firing fast-twitch fibers. It is concluded that regulation of Gm is a general phenomenon in AP-firing muscle, and that differences in Gm regulation may contribute to the different phenotypes of fast- and slow-twitch muscle.

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