Attractin deficiency causes metabolic and morphological abnormalities in slow-twitch muscle

Author(s):  
Ayuka Ehara ◽  
Daisuke Taguchi ◽  
Kazuhiko Nakadate ◽  
Shuichi Ueda
Author(s):  
Wanxue Wen ◽  
Xiaoling Chen ◽  
Zhiqing Huang ◽  
Daiwen Chen ◽  
Bing Yu ◽  
...  

Cells ◽  
2018 ◽  
Vol 7 (12) ◽  
pp. 243 ◽  
Author(s):  
Manting Ma ◽  
Bolin Cai ◽  
Liang Jiang ◽  
Bahareldin Ali Abdalla ◽  
Zhenhui Li ◽  
...  

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.


1987 ◽  
Vol 253 (3) ◽  
pp. C426-C432 ◽  
Author(s):  
D. M. Whitlock ◽  
R. L. Terjung

Rat slow-twitch muscle, in contrast to fast-twitch muscle, maintains its ATP content near normal during intense stimulation conditions that produce rapid fatigue. An extensive depletion of adenine nucleotide content by the deamination of AMP to IMP + NH3, typical of fast-twitch muscle, does not occur. We evaluated whether this response of slow-twitch muscle could be simply due to failure of synaptic transmission or related to cellular conditions influencing enzyme activity. Stimulation of soleus muscles in situ via the nerve or directly in the presence of curare at 120 tetani/min for 3 min resulted in extensive fatigue but normal ATP contents. Thus the lack of ATP depletion must be related to cellular events distal to neuromuscular transmission. Even nerve and direct muscle stimulation (with curare) during ischemia did not cause a large depletion of ATP or a large elevation of lactate content (12.0 +/- 0.7 mumol/g), even though the decline in tension was essentially complete. However, if the same tension decline during ischemia was prolonged by stimulating for 10 min at 12 tetani/min a large decrease in ATP (2.24 +/- 0.09 mumol/g) and increase in IMP (2.47 +/- 0.16 mumol/g) and lactate (30.4 +/- 2.0 mumol/g) content occurred. Thus adenine nucleotide deamination to IMP can occur in slow-twitch muscle during specific contraction conditions. The cellular events leading to the activation of AMP deaminase require an intense contraction condition and may be related to acidosis caused by a high lactate content.


1983 ◽  
Vol 61 (2) ◽  
pp. 217-233 ◽  
Author(s):  
John A. Pizzey ◽  
Eric A. Barnard ◽  
Penelope J. Barnard

2004 ◽  
Vol 96 (3) ◽  
pp. 1039-1044 ◽  
Author(s):  
Paul McDonough ◽  
Brad J. Behnke ◽  
Timothy I. Musch ◽  
David C. Poole

The speed with which muscle energetic status recovers after exercise is dependent on oxidative capacity and vascular O2 pressures. Because vascular control differs between muscles composed of fast- vs. slow-twitch fibers, we explored the possibility that microvascular O2 pressure (PmvO2; proportional to the O2 delivery-to-O2 uptake ratio) would differ during recovery in fast-twitch peroneal (Per: 86% type II) compared with slow-twitch soleus (Sol: 84% type I). Specifically, we hypothesized that, in Per, PmvO2 would be reduced immediately after contractions and would recover more slowly during the off-transient from contractions compared with Sol. The Per and Sol muscles of six female Sprague-Dawley rats (weight = ∼220 g) were studied after the cessation of electrical stimulation (120 s; 1 Hz) to compare the recovery profiles of PmvO2. As hypothesized, PmvO2 was lower throughout recovery in Per compared with Sol (end contraction: 13.4 ± 2.2 vs. 20.2 ± 0.9 Torr; end recovery: 24.0 ± 2.4 vs. 27.4 ± 1.2 Torr, Per vs. Sol; P ≤ 0.05). In addition, the mean response time for recovery was significantly faster for Sol compared with Per (45.1 ± 5.3 vs. 66.3 ± 8.1 s, Sol vs. Per; P < 0.05). Despite these findings, PmvO2 rose progressively in both muscles and at no time fell below end-exercise values. These data indicate that, during the recovery from contractions (which is prolonged in Per), capillary O2 driving pressure (i.e., PmvO2) is reduced in fast-compared with slow-twitch muscle. In conclusion, the results of the present investigation may partially explain the slowed recovery kinetics (phosphocreatine and O2 uptake) found previously in 1) fast- vs. slow-twitch muscle and 2) various patient populations, such as those with congestive heart failure and diabetes mellitus.


Sign in / Sign up

Export Citation Format

Share Document