scholarly journals Osteopontin deficiency delays inflammatory infiltration and the onset of muscle regeneration in a mouse model of muscle injury

2012 ◽  
Vol 6 (1) ◽  
pp. 197-205 ◽  
Author(s):  
K. Uaesoontrachoon ◽  
D. K. Wasgewatte Wijesinghe ◽  
E. J. Mackie ◽  
C. N. Pagel
2021 ◽  
Author(s):  
Sanzana Hoque ◽  
Rana Soylu Kucharz ◽  
Valérie Allamand ◽  
Marie Sjögren ◽  
Kinga Gawlik ◽  
...  

2019 ◽  
Author(s):  
Xueyuan Hu ◽  
Yonghui Yu ◽  
Junxia Feng ◽  
Mengjiao Fu ◽  
Lupeng Dai ◽  
...  

Abstract Background: Q fever is a worldwide zoonosis caused by Coxiella burnetii and mainly transmitted by aerosols. This study aims at establishing a systematic and efficient mouse model of acute Q fever via intratracheal (IT) inoculation of aerosolized C. burnetii. Methods: BALB/c mice were infected with C. burnetii via IT route using a non-invasive aerosol pulmonary delivery device to directly place the living C. burnetii organisms into their tracheas. The bacterial loads, pathological lesions, and serological responses were analyzed in mice, and compared with those of mice infected via intraperitoneal (IP) route. Results: As early as at day three post-infection (pi) with a low dose of C. burnetii (1×10⁴ per mouse), a large amount of C. burnetii organisms were determined in blood, lungs, hearts, livers, and spleens of the mice. The inflammatory infiltration was observed in hearts and lungs of mice. Compared with mice infected via IP route, the mice infected via IT route exhibited a higher level of bacterial loads and more severe pathological lesions in hearts and lungs at day 3 and day 7 pi. Conclusions: These data indicated that IT route is more efficient than IP route to cause acute C. burnetii infection in mice. Overall, we successfully established a mouse model of C. burnetii infection via IT route, which is useful for investigations of pathogenesis and immunity of acute C. burnetii infection as well as evaluation of therapeutic drugs and preventive vaccines of Q fever.


2020 ◽  
Author(s):  
Iwona Bronisz-Budzyńska ◽  
Magdalena Kozakowska ◽  
Paulina Podkalicka ◽  
Neli Kachamakova-Trojanowska ◽  
Agnieszka Łoboda ◽  
...  

Abstract The nuclear factor erythroid 2-related factor 2 (Nrf2) is considered as a master cytoprotective factor regulating the expression of genes encoding anti-oxidant, anti-inflammatory, and detoxifying proteins. The role of Nrf2 in the pathophysiology of skeletal muscles has been evaluated in different experimental models, however, due to inconsistent data, we aimed to investigate how Nrf2 transcriptional deficiency (Nrf2tKO) affects muscle functions both in an acute and chronic injury. The acute muscle damage was induced in mice of two genotypes – WT and Nrf2tKO mice by cardiotoxin (CTX) injection. To investigate the role of Nrf2 in chronic muscle pathology, mdx mice that share genetic, biochemical, and histopathological features with Duchenne muscular dystrophy (DMD) were crossed with mice lacking transcriptionally active Nrf2 and double knockouts (mdx/Nrf2tKO) were generated. To worsen the dystrophic phenotype, the analysis of disease pathology was also performed in aggravated conditions, by applying a long-term treadmill test.We have observed slightly increased muscle damage in Nrf2tKO mice after CTX injection. Nevertheless, transcriptional ablation of Nrf2 in mdx mice did not significantly aggravate the most deleterious, pathological hallmarks of DMD related to degeneration, inflammation, fibrotic scar formation, angiogenesis, and the number and proliferation of satellite cells in non-exercised conditions. On the other hand, upon chronic exercises, the degeneration and inflammatory infiltration of the gastrocnemius muscle, but not diaphragm, turned to be increased in Nrf2tKOmdx in comparison to mdx mice. In conclusion, the lack of transcriptionally active Nrf2 influences moderately muscle pathology in acute CTX-induced muscle injury and chronic DMD mouse model, without affecting muscle functionality. Hence, in general, we demonstrated that the deficiency of Nrf2 transcriptional activity has no profound impact on muscle pathology in various models of muscle injury.


2018 ◽  
Vol 46 (6) ◽  
pp. 2271-2283 ◽  
Author(s):  
Lianjie Hou ◽  
Jian Xu ◽  
Yiren Jiao ◽  
Huaqin Li ◽  
Zhicheng Pan ◽  
...  

Background/Aims: Skeletal muscle plays an essential role in the body movement. However, injuries to the skeletal muscle are common. Lifelong maintenance of skeletal muscle function largely depends on preserving the regenerative capacity of muscle. Muscle satellite cells proliferation, differentiation, and myoblast fusion play an important role in muscle regeneration after injury. Therefore, understanding of the mechanisms associated with muscle development during muscle regeneration is essential for devising the alternative treatments for muscle injury in the future. Methods: Edu staining, qRT-PCR and western blot were used to evaluate the miR-27b effects on pig muscle satellite cells (PSCs) proliferation and differentiation in vitro. Then, we used bioinformatics analysis and dual-luciferase reporter assay to predict and confirm the miR-27b target gene. Finally, we elucidate the target gene function on muscle development in vitro and in vivo through Edu staining, qRT-PCR, western blot, H&E staining and morphological observation. Result: miR-27b inhibits PSCs proliferation and promotes PSCs differentiation. And the miR-27b target gene, MDFI, promotes PSCs proliferation and inhibits PSCs differentiation in vitro. Furthermore, interfering MDFI expression promotes mice muscle regeneration after injury. Conclusion: our results conclude that miR-27b promotes PSCs myogenesis by targeting MDFI. These results expand our understanding of muscle development mechanism in which miRNAs and genes work collaboratively in regulating skeletal muscle development. Furthermore, this finding has implications for obtaining the alternative treatments for patients with the muscle injury.


2021 ◽  
Author(s):  
Kentaro Fukuda ◽  
Taisuke Kuroda ◽  
Norihisa Tamura ◽  
Hiroshi Mita ◽  
Hirofumi Miyata ◽  
...  

2019 ◽  
Vol 6 (3) ◽  
pp. e561 ◽  
Author(s):  
Wenli Zhu ◽  
Zhen Wang ◽  
Suying Hu ◽  
Ye Gong ◽  
Yuanchu Liu ◽  
...  

ObjectiveUsing phage display, we sought to screen single-chain variable fragments (scFvs) against complement C5 to treat neuromyelitis optica spectrum disorder (NMOSD).MethodsAfter 5 rounds of phage display, we isolated individual clones and identified phage clones specifically binding to C5 using ELISA. Using aquaporin-4 (AQP4)-transfected cells in vitro, we confirmed whether these scFvs prevented complement-dependent cytotoxicity (CDC) caused by the serum of patients with NMOSD and human complement (hC). We selected an NMOSD mouse model, in which intracerebral NMOSD immunoglobulin G (IgG) and hC injections induce NMOSD-like lesions in vivo.ResultsWe obtained scFvs to test specificity and blocking efficiency. The scFv C5B3 neutralized C5 in the complement activation pathway, which prevented AQP4-IgG–mediated CDC in AQP4-transfected cells. In an NMOSD mouse model, C5B3 prevented AQP4 and astrocyte loss, decreased demyelination, and reduced inflammatory infiltration and membrane attack complex formation in lesions.ConclusionsWe used phage display to screen C5B3 against C5, which was effective in inhibiting cytotoxicity in vitro and preventing CNS pathology in vivo.


Life Sciences ◽  
2019 ◽  
Vol 235 ◽  
pp. 116835 ◽  
Author(s):  
Deng-Fa Yang ◽  
Ying-Ling Shen ◽  
Changwei Wu ◽  
Yu-Sheng Huang ◽  
Po-Ying Lee ◽  
...  

2016 ◽  
Vol 32 (2) ◽  
pp. 317-325 ◽  
Author(s):  
Samuel Rodrigues Lourenço Morais ◽  
Alexandre Ginei Goya ◽  
Úrsula Urias ◽  
Paulo Roberto Jannig ◽  
Aline Villa Nova Bacurau ◽  
...  

PM&R ◽  
2014 ◽  
Vol 6 (8) ◽  
pp. S95 ◽  
Author(s):  
Kunj G. Patel ◽  
Makoto Kobayashi ◽  
Tom Best ◽  
Johnny Huard

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