FGF6 enhances muscle regeneration after nerve injury by relying on ERK1/2 mechanism

Cai, Qiu-Chen; Wu, Guangjie; Min, Zhu; Ge, Heng’an; Xue, Chao; Zhang, Qing'’gang; Cheng, Biao; Xu, Shouping; Wu, Peng

doi:10.1016/j.lfs.2020.117465

Cited by 17 publications

(14 citation statements)

References 30 publications

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“…Previous studies have shown that the MAPK signaling pathway is a key step in myogenesis, including ERK and P38, and its role in myogenesis has been extensively studied. [45][46][47][48] Besides, various stimuli, such as inflammatory cytokines, tumor necrosis factors, and growth factors, can activate the MAPK pathway in satellite cells. In some studies, the inhibitors of the MAPK pathway are used to prevent the fusion of muscle cells into myotubes and the induction of muscle-specific genes, 49 whereas some constitutively active mutants, such as the ectopic expression of MKK6, can be forced to activate the MAPK signaling pathway, which would induce the expression of myocyte differentiation markers and the appearance of multinucleated myotubes.…”

Section: Discussionmentioning

confidence: 99%

LncRNA XLOC_015548 affects the proliferation and differentiation of myoblasts via the MAPK signaling pathway

Wei

Cao

et al. 2023

Exp Biol Med (Maywood)

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In recent years, an increasing number of studies have reported that long non-coding RNAs (lncRNAs) play essential regulatory roles in myogenic differentiation. In this study, a specific LncRNA XLOC_015548 (Lnc000280) was identified. However, little research has explored its mechanism of action by constructing XLOC_015548 gene editing cell models. In this study, relevant sequences were obtained according to the RNA-seq results. Subsequently, XLOC_015548 knockdown and over-expression lentiviral vectors were constructed, and the C2C12 myoblast cell line was transfected to prepare the XLOC_015548 gene-edited myoblast model. The in vitro analysis revealed that over-expression of XLOC_015548 significantly promoted the proliferation and differentiation of myoblasts and the formation of myotubes, whereas the opposite result was obtained in the knockdown group. XLOC_015548 regulated myogenic differentiation and affected the expression of myogenic differentiation regulators such as Myod, myogenin, and MyHC. Regarding the signaling pathway, we found that XLOC_015548 correlated with the phosphorylation level of MAPK/MEK/ERK pathway proteins. And the degree of phosphorylation was positively correlated with the protein expression of myogenic differentiation regulators. In conclusion, a new gene-edited myoblast model was constructed based on the lncRNA regulator XLOC_015548. The in vitro cell experiments verified that XLOC_015548 had regulatory effects on muscle growth and myoblast differentiation. These findings provide a laboratory foundation for the clinical application of lncRNAs as regulatory factors in the treatment of disuse muscle atrophy.

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Section: Discussionmentioning

confidence: 99%

LncRNA XLOC_015548 affects the proliferation and differentiation of myoblasts via the MAPK signaling pathway

Wei

Cao

et al. 2023

Exp Biol Med (Maywood)

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“…We noticed that FGF6 could activate the mitogen‐activated protein kinase signalling pathway and promote activation of ERK1/2. ERK1/2 is one of the mitogen‐activated protein kinases 27,34 the key components of the reperfusion injury salvage kinase pathway, and plays an important role in protecting the myocardium from lethal ischemia–reperfusion injury. Constitutive activation of mitogen‐activated protein kinase 1 (CaMEK) promotes ERK1/2 expression, which is expected to protect the heart against ischemia–reperfusion injury 25,27 .…”

Section: Discussionmentioning

confidence: 99%

“…[29][30][31] FGF6 expression is stimulated after skeletal muscle injury and can promote skeletal muscle regeneration, whereas interference of FGF6 can induce a severe regeneration defect with enhanced fibrosis and myotube degeneration. [32][33][34] FGF6 plays a similar role in repair following myocardial injury. In this study, we revealed that FGF6 expression was elevated in ischemic CMs and cardiac tissues.…”

Section: Discussionmentioning

confidence: 99%

FGF6 promotes cardiac repair after myocardial infarction by inhibiting the Hippo pathway

Chen

Wang

et al. 2022

Cell Proliferation

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Objectives: Myocardial infarction (MI) commonly occurs in patients with coronary artery disease and have high mortality. Current clinical strategies for MI still limited to reducing the death of myocardial cells but failed to replace these cells. This study aimed to investigate the role of fibroblast growth factor 6 (FGF6) in enhancing the proliferative potential of cardiomyocytes (CMs) after ischemic injury via the Hippo pathway.Materials and Methods: Expression of FGF6 protein was analysed in mice with MI induced by ligation of the left anterior descending coronary artery. Activation of the Hippo pathway and the proliferation potential were examined in ischemic CMs, treated with FGF6 protein or transfected with an adeno-virus carrying FGF6 sh-RNA.Immunofluorescence staining and western blotting were performed to assess the relationship between FGF6 and the Hippo pathway.Results: We found that FGF6 expression was significantly increased in the MI mouse model. Knockdown of FGF6 synthesis resulted in poorer heart function after MI. By contrast, treatment with recombinant human FGF6 protein improved heart function, reduced infarct size, and promoted cardiac repair. Additionally, FGF6 restrains the activation of the Hippo pathway and subsequently promotes nuclear accumulation of YAP. This was largely counteracted by treatment with extracellular signal-regulated kinase 1/2 (ERK1/2) inhibitor U0126.

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“…The static stretching prior to the ladder-based resistance training revealed an increase in the FGF-6 expression at the MTJ. Cai et al (2020) showed that the FGF-6 protein increased cell migration and differentiation in tibialis anterior muscle's cell culture. In a previous paper, we revealed that static stretching prior to body-weight training increased the gastrocnemius muscle myofibers’ number, possibly by the increased length (Barbosa et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

Ultrastructural and Molecular Development of the Myotendinous Junction Triggered by Stretching Prior to Resistance Exercise

et al. 2022

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The myotendinous junction (MTJ) is a highly specialized region of the locomotor apparatus. Here, we investigated the ultrastructural and molecular effects in the MTJ region after static stretching prior to the ladder-based resistance training. Thirty-two male, 60-day old Wistar rats were divided into four groups: Sedentary, Resistance Training, Stretching, and Stretching-Resistance Training. The gastrocnemius muscle was processed for transmission electron microscopy techniques and Western blot assay. We observed that the static stretching prior to the ladder-based resistance training increased the MTJ components, the fibroblast growth factor (FGF)-2 and FGF-6 protein expression. Also, we demonstrated the lower transforming growth factor expression and no difference in the lysyl oxidase expression after combined training. The MTJ alterations in response to combined training demonstrate adaptive mechanisms which can be used for the prescription or development of methods to reduce or prevent injuries in humans and promote the myotendinous interface benefit.

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FGF6 enhances muscle regeneration after nerve injury by relying on ERK1/2 mechanism

Cited by 17 publications

References 30 publications

LncRNA XLOC_015548 affects the proliferation and differentiation of myoblasts via the MAPK signaling pathway

LncRNA XLOC_015548 affects the proliferation and differentiation of myoblasts via the MAPK signaling pathway

FGF6 promotes cardiac repair after myocardial infarction by inhibiting the Hippo pathway

Ultrastructural and Molecular Development of the Myotendinous Junction Triggered by Stretching Prior to Resistance Exercise

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