Immediate and delayed transplantation of mesenchymal stem cells improve muscle force after skeletal muscle injury in rats

2012 ◽  
Vol 6 (S3) ◽  
pp. s60-s67 ◽  
Author(s):  
Tobias Winkler ◽  
Philipp von Roth ◽  
Piotr Radojewski ◽  
Alexander Urbanski ◽  
Sebastian Hahn ◽  
...  
2010 ◽  
Vol 16 (9) ◽  
pp. 2871-2881 ◽  
Author(s):  
Edward K. Merritt ◽  
Megan V. Cannon ◽  
David W. Hammers ◽  
Long N. Le ◽  
Rohit Gokhale ◽  
...  

2019 ◽  
Vol 20 (17) ◽  
pp. 4312 ◽  
Author(s):  
Wen-Hong Su ◽  
Ching-Jen Wang ◽  
Hung-Chun Fu ◽  
Chien-Ming Sheng ◽  
Ching-Chin Tsai ◽  
...  

Skeletal muscle injury presents a challenging traumatological dilemma, and current therapeutic options remain mediocre. This study was designed to delineate if engraftment of mesenchymal stem cells derived from umbilical cord Wharton’s jelly (uMSCs) could aid in skeletal muscle healing and persuasive molecular mechanisms. We established a skeletal muscle injury model by injection of myotoxin bupivacaine (BPVC) into quadriceps muscles of C57BL/6 mice. Post BPVC injection, neutrophils, the first host defensive line, rapidly invaded injured muscle and induced acute inflammation. Engrafted uMSCs effectively abolished neutrophil infiltration and activation, and diminished neutrophil chemotaxis, including Complement component 5a (C5a), Keratinocyte chemoattractant (KC), Macrophage inflammatory protein (MIP)-2, LPS-induced CXC chemokine (LIX), Fractalkine, Leukotriene B4 (LTB4), and Interferon-γ, as determined using a Quantibody Mouse Cytokine Array assay. Subsequently, uMSCs noticeably prevented BPVC-accelerated collagen deposition and fibrosis, measured by Masson’s trichrome staining. Remarkably, uMSCs attenuated BPVC-induced Transforming growth factor (TGF)-β1 expression, a master regulator of fibrosis. Engrafted uMSCs attenuated TGF-β1 transmitting through interrupting the canonical Sma- And Mad-Related Protein (Smad)2/3 dependent pathway and noncanonical Smad-independent Transforming growth factor beta-activated kinase (TAK)-1/p38 mitogen-activated protein kinases signaling. The uMSCs abrogated TGF-β1-induced fibrosis by reducing extracellular matrix components including fibronectin-1, collagen (COL) 1A1, and COL10A1. Most importantly, uMSCs modestly extricated BPVC-impaired gait functions, determined using CatWalk™ XT gait analysis. This work provides several innovative insights into and molecular bases for employing uMSCs to execute therapeutic potential through the elimination of neutrophil-mediated acute inflammation toward protecting against fibrosis, thereby rescuing functional impairments post injury.


2009 ◽  
Vol 28 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Andres J. Quintero ◽  
Vonda J. Wright ◽  
Freddie H. Fu ◽  
Johnny Huard

2020 ◽  
Vol 17 (6) ◽  
pp. 887-900
Author(s):  
Manal H. Moussa ◽  
Ghada G. Hamam ◽  
Asmaa E. Abd Elaziz ◽  
Marwa A. Rahoma ◽  
Abeer A. Abd El Samad ◽  
...  

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