Dhx36 promotes satellite cell proliferation during skeletal muscle regeneration by binding 5' UTR G-quadruplex of mRNAs and facilitating translation

Author(s):  
Xiaona Chen
2015 ◽  
Vol 309 (3) ◽  
pp. C159-C168 ◽  
Author(s):  
Tsung-Chuan Ho ◽  
Yi-Pin Chiang ◽  
Chih-Kuang Chuang ◽  
Show-Li Chen ◽  
Jui-Wen Hsieh ◽  
...  

In response injury, intrinsic repair mechanisms are activated in skeletal muscle to replace the damaged muscle fibers with new muscle fibers. The regeneration process starts with the proliferation of satellite cells to give rise to myoblasts, which subsequently differentiate terminally into myofibers. Here, we investigated the promotion effect of pigment epithelial-derived factor (PEDF) on muscle regeneration. We report that PEDF and a synthetic PEDF-derived short peptide (PSP; residues Ser93-Leu112) induce satellite cell proliferation in vitro and promote muscle regeneration in vivo. Extensively, soleus muscle necrosis was induced in rats by bupivacaine, and an injectable alginate gel was used to release the PSP in the injured muscle. PSP delivery was found to stimulate satellite cell proliferation in damaged muscle and enhance the growth of regenerating myofibers, with complete regeneration of normal muscle mass by 2 wk. In cell culture, PEDF/PSP stimulated C2C12 myoblast proliferation, together with a rise in cyclin D1 expression. PEDF induced the phosphorylation of ERK1/2, Akt, and STAT3 in C2C12 myoblasts. Blocking the activity of ERK, Akt, or STAT3 with pharmacological inhibitors attenuated the effects of PEDF/PSP on the induction of C2C12 cell proliferation and cyclin D1 expression. Moreover, 5-bromo-2′-deoxyuridine pulse-labeling demonstrated that PEDF/PSP stimulated primary rat satellite cell proliferation in myofibers in vitro. In summary, we report for the first time that PSP is capable of promoting the regeneration of skeletal muscle. The signaling mechanism involves the ERK, AKT, and STAT3 pathways. These results show the potential utility of this PEDF peptide for muscle regeneration.


2013 ◽  
Vol 288 (33) ◽  
pp. 23823-23832 ◽  
Author(s):  
Tadashi Yoshida ◽  
Sarah Galvez ◽  
Sumit Tiwari ◽  
Bashir M. Rezk ◽  
Laura Semprun-Prieto ◽  
...  

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Matthew J. Mervis ◽  
Marc S. Matsumura ◽  
Zachary E. Olsen ◽  
Kelsey M. Hirschi-Budge ◽  
Paul R. Reynolds ◽  
...  

2011 ◽  
Vol 1 (1) ◽  
pp. 33 ◽  
Author(s):  
Alison R Angione ◽  
Chunhui Jiang ◽  
Dongning Pan ◽  
Yong-Xu Wang ◽  
Shihuan Kuang

2001 ◽  
Vol 189 (2) ◽  
pp. 189-196 ◽  
Author(s):  
Marie Csete ◽  
Jean Walikonis ◽  
Nicole Slawny ◽  
Yuewang Wei ◽  
Sheryl Korsnes ◽  
...  

2001 ◽  
Vol 90 (4) ◽  
pp. 1407-1414 ◽  
Author(s):  
Heather K. Smith ◽  
Linda Maxwell ◽  
Carol D. Rodgers ◽  
Nancy H. McKee ◽  
Michael J. Plyley

The effects of increased functional loading on early cellular regenerative events after exercise-induced injury in adult skeletal muscle were examined with the use of in vivo labeling of replicating myofiber nuclei and immunocyto- and histochemical techniques. Satellite cell proliferation in the soleus (Sol) of nonexercised rats (0.4 ± 0.2% of fibers) was unchanged after an initial bout of declined treadmill exercise but was elevated after two (1.0 ± 0.2%, P ≤ 0.01), but not four or seven, daily bouts of the same task. Myonuclei produced over the 7-day period comprised 0.9–1.9% of myonuclei in isolated fibers of Sol, tibialis anterior, and vastus intermedius of nonexercised rats. The accretion of new myonuclei was enhanced ( P ≤ 0.05) in Sol and vastus intermedius by the initial exercise followed by normal activity (to 3.1–3.4% of myonuclei) and more so by continued daily exercise (4.2–5.3%). Observed coincident with a lower incidence of histological fiber injury and unchanged fiber diameter and myonuclei per millimeter, the greater new myonuclear accretion induced by continued muscle loading may contribute to an enhanced fiber repair and regeneration after exercise-induced injury.


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