Mitsugumin 53 promotes mitochondrial autophagy through regulating Ambra1 expression in C2C12 myoblast cells

2019 ◽  
Vol 43 (3) ◽  
pp. 290-298 ◽  
Author(s):  
Gu Lijie ◽  
Zhang Yueyue ◽  
Zhu Nan ◽  
Wang Ling ◽  
Wang Xuan ◽  
...  
Keyword(s):  
C2c12 Myoblast ◽  
Myoblast Cells

scholarly journals Osteocalcin Induces Proliferation via Positive Activation of the PI3K/Akt, P38 MAPK Pathways and Promotes Differentiation Through Activation of the GPRC6A-ERK1/2 Pathway in C2C12 Myoblast Cells

2017 ◽  
Vol 43 (3) ◽  
pp. 1100-1112 ◽  
Author(s):  
Suifeng Liu ◽  
Feng Gao ◽  
Lei Wen ◽  
Min Ouyang ◽  
Yi Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
P38 Mapk ◽  
C2c12 Cell ◽  
C2c12 Cells ◽  
Myoblast Differentiation ◽  
C2c12 Myoblast ◽  
C2c12 Myoblasts ◽  
Mapk Phosphorylation ◽  
Mapk Pathways ◽  
Myoblast Cells

Background/Aims: Sarcopenia is characterized by an age-related decline in skeletal muscle plus low muscle strength and/or physical performance. Despite the clinical significance of sarcopenia, the molecular pathways underlying sarcopenia remain elusive. The recent demonstration that undercarboxylated osteocalcin (ucOC) favours muscle function related to insulin sensitivity and glucose metabolism raises the question of whether this hormone may also regulate muscle mass. The present study explored the promotive effects of ucOC in proliferation and differentiation processes of C2C12 myoblasts as well as the possible signalling pathways involved. Methods: The effects of exogenous ucOC on C2C12 myoblasts proliferation were assessed using CCK8 and immunohistological staining assays. C2C12 cells were pretreated with PI3K/Akt or P38 MAPK inhibitors to investigate the possible involvement of the PI3K/Akt and P38 MAPK pathways in proliferation. The levels of Akt, phosphorylated-Akt (p-Akt), P38, and phosphorylated-P38 (p-P38) were measured by Western Blotting. The effects of ucOC on myoblast differentiation were quantified by morphological analysis. A silencing experiment was conducted in which the expression of GPRC6A in C2C12 myoblasts was modified. The expression of GPRC6A, myosin heavy chain (MyHC) and the related ERK1/2 signalling pathway in C2C12 myoblasts were monitored by qRT-PCR and Western Blotting. Results: We showed that treatment with exogenous ucOC stimulated the priming of C2C12 myoblasts proliferation. Inhibition of Akt phosphorylation by wortmannin or inhibition of P38 MAPK phosphorylation by SB203580 decreased C2C12 cell proliferation. Wortmannin also reduced P38 MAPK phosphorylation, whereas SB203580 did not affect Akt activation. Furthermore, ucOC promoted C2C12 myoblast differentiation. Inhibition of ERK1/2 phosphorylation with U0126 decreased C2C12 cell differentiation. Finally, GPRC6A expression was substantially increased after ucOC treatment of C2C12 cells. GPRC6A silencing inhibited Akt, P38 MAPK phosphorylation in C2C12 cells, and ERK1/2 phosphorylation in C2C12 myotubes; GPRC6A silencing also decreased cell proliferation, decreased cell differentiation, and downregulated MyHC expression. Conclusions: The present data suggest that ucOC induces myoblast proliferation via sequential activation of the PI3K/Akt and p38 MAPK pathways in C2C12 myoblast cells. Moreover, ucOC enhances myogenic differentiation via a mechanism involving GPRC6A-ERK1/2 signalling.

scholarly journals Nogo-A is critical for pro-inflammatory gene regulation in myocytes and macrophages

2020 ◽  
Author(s):  
H M Arif Ullah ◽  
A. K. Elfadl ◽  
SunYoung Park ◽  
Yong Deuk Kim ◽  
Myung-Jin Chung ◽  
...  
Keyword(s):  
Inflammatory Process ◽  
Vital Role ◽  
C2c12 Cells ◽  
Inflammatory Factors ◽  
Mdx Mice ◽  
C2c12 Myoblast ◽  
Homologous Protein ◽  
Inflammatory Processes ◽  
Myoblast Cells ◽  
Factor C

Abstract Background: Nogo-A (Rtn 4A), a member of the reticulon 4 (Rtn4) protein family, is a neurite outgrowth inhibitor protein that is primarily expressed in the central nervous system (CNS). However, the role of Nogo-A in inflammatory mechanisms remains unclear. Therefore, in this study, we used Nogo-knockout (KO) mice to explore its potential role in the inflammatory process. Here, we investigated whether Nogo-A affects the inflammatory process through transcription factor C/EBP homologous protein (CHOP). Results: Our results demonstrated that Nogo-A, CHOP, and pro-inflammatory factors were activated in the following: notexin-induced muscle injury, in human Duchenne muscular dystrophy (DMD) patients, in dystrophin-deficient (mdx) mice, in differentiated C2C12 myoblast cells, and in lipopolysaccharide (LPS)-stimulated bone marrow-derived macrophages (BMDM). Moreover, we found that Nogo-KO BMDM exhibited lower migratory ability compared with wild type (WT) BMDM after LPS treatment. Conclusion: Our data demonstrated that the Nogo-A-CHOP signaling pathway regulated the inflammatory process in notexin-induced injured muscle, in mdx mice, in DMD patients, in differentiated C2C12 cells, and in LPS-stimulated BMDM. Taken together, these results suggest that Nogo-A plays a vital role in inflammatory processes, which resembles the pathological mechanisms observed in the CNS.

scholarly journals Lipid droplets contribute myogenic differentiation in C2C12 by promoting the remodeling of the acstin-filament

2021 ◽  
Vol 12 (12) ◽  
Author(s):  
Yanjie Tan ◽  
Yi Jin ◽  
Pengxiang Zhao ◽  
Jian Wu ◽  
Zhuqing Ren
Keyword(s):  
Skeletal Muscle ◽  
Actin Filaments ◽  
Lipid Droplets ◽  
Myogenic Differentiation ◽  
C2c12 Myoblast ◽  
Cellular Processes ◽  
Myoblast Cells ◽  
Athlete’S Paradox ◽  
The Impact ◽  
Insight Into

AbstractLipid droplet (LD), a multi-functional organelle, is found in most eukaryotic cells. LDs participate in the regulation of many cellular processes including proliferation, stress, and apoptosis. Previous studies showed the athlete’s paradox that trained athletes accumulate LDs in their skeletal muscle. However, the impact of LDs on skeletal muscle and myogenesis is not clear. We discovered that C2C12 myoblast cells containing more LDs formed more multinucleated muscle fibers. We also discovered that LDs promoted cell migration and fusion by promoting actin-filaments remodeling. Mechanistically, two LD-proteins, Acyl-CoA synthetase long chain family member 3 (ACSL3) and lysophosphatidylcholine acyltransferase 1 (LPCAT1), medicated the recruitment of actinin proteins which contributed to actin-filaments formation on the surface of LDs. During remodeling, the actinin proteins on LDs surface translocated to actin-filaments via ARF1/COPI vesicles. Our study demonstrate LDs contribute to cell differentiation, which lead to new insight into the LD function.

Oleate Ameliorates Palmitate-Induced Impairment of Differentiative Capacity in C2C12 Myoblast Cells

2021 ◽  
Author(s):  
Mengjuan Xue ◽  
Fan Zhang ◽  
Xueying Ji ◽  
Huiyuan Yu ◽  
Xin Jiang ◽  
...  
Keyword(s):  
C2c12 Myoblast ◽  
Myoblast Cells

Effects of inorganic phosphate and FGF23 on C2C12 myoblast cells

2015 ◽  
Author(s):  
Adalbert Raimann ◽  
Alexander Dangl ◽  
Susanne Sagmeister ◽  
Susanne Greber-Platzer ◽  
Gabriele Haeusler
Keyword(s):  
Inorganic Phosphate ◽  
C2c12 Myoblast ◽  
Myoblast Cells

scholarly journals Simvastatin suppresses the differentiation of C2C12 myoblast cells via a Rac pathway

2008 ◽  
Vol 29 (2-5) ◽  
pp. 127-134 ◽  
Author(s):  
Tomomi T. Baba ◽  
Takayuki K. Nemoto ◽  
Toshihiro Miyazaki ◽  
Shinichiro Oida
Keyword(s):  
C2c12 Myoblast ◽  
Myoblast Cells

scholarly journals Resveratrol Decreases Oxidative Stress by Restoring Mitophagy and Improves the Pathophysiology of Dystrophin-Deficient mdx Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Rio Sebori ◽  
Atsushi Kuno ◽  
Ryusuke Hosoda ◽  
Takashi Hayashi ◽  
Yoshiyuki Horio
Keyword(s):  
Creatine Kinase ◽  
Therapeutic Agent ◽  
Serum Creatine Kinase ◽  
Physical Activities ◽  
Mdx Mice ◽  
C2c12 Myoblast ◽  
Autophagic Flux ◽  
Oxygen Species ◽  
Central Nuclei ◽  
Myoblast Cells

We previously showed that treatment with resveratrol (3,5,4′-trihydroxy-trans-stilbene), an activator of the NAD+-dependent deacetylase SIRT1 at 4 g/kg food for 32 weeks, significantly decreased the muscular reactive oxygen species (ROS) levels and ameliorated the pathology of mdx mice, an animal model of Duchenne muscular dystrophy (DMD). Here, we treated mdx mice with various doses of resveratrol (0.04, 0.4, and 4 g/kg food) for 56 weeks and examined the effects on serum creatine kinase levels and physical activities. Because resveratrol promotes autophagy, we also investigated whether autophagy including mitochondrial autophagy (mitophagy) is involved in resveratrol’s effects. Autophagy/mitophagy-related genes and autophagic flux were downregulated in the muscle of mdx mice, and these phenomena were reversed by resveratrol with significant ROS reduction. Resveratrol at 4 g/kg food reduced the number of immature myofibers containing central nuclei and fine fibers < 400 μm2 and increased that of thicker myofibers in the quadriceps, suggesting that resveratrol decreased myofiber wasting and promoted muscular maturation. Accordingly, resveratrol at 0.4 g/kg food reduced the creatine kinase levels to one-third of those in untreated mdx mice and significantly increased the animals’ physical activities. In C2C12 myoblast cells, resveratrol promoted mitophagy and eliminated mitochondria containing high superoxide levels. The clearance of damaged mitochondria and ROS reduction by resveratrol was completely suppressed by an autophagy inhibitor (chloroquine) and by knocking down Atg5 or Pink1, essential genes for autophagy and mitophagy, respectively. Thus, resveratrol is a potential therapeutic agent for DMD, and the clearance of damaged mitochondria probably contributes to its action.

Ethanol extract of Cyclolepis genistoides D. Don (palo azul) induces formation of myotubes, which involves differentiation of C2C12 myoblast cells

2016 ◽  
Vol 36 (7) ◽  
pp. 731-741 ◽  
Author(s):  
Hiromi Sato ◽  
Asami Funaki ◽  
Yuki Kimura ◽  
Mai Sumitomo ◽  
Hiroya Yoshida ◽  
...  
Keyword(s):  
Ethanol Extract ◽  
C2c12 Myoblast ◽  
Myoblast Cells
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