FHL1 regulates myoblast differentiation and autophagy through its interaction with LC3

Han, Shunshun; Cui, Can; He, Haorong; Shen, Xiaoxu; Chen, Yuqi; Wang, Yan; Li, Diyan; Zhu, Qing; Yin, Huadong

doi:10.1002/jcp.29345

Cited by 24 publications

(22 citation statements)

References 42 publications

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“…CSRP3 (Rashid et al, 2015) and FHL1 (Han et al, 2020) have been recently found to interact with LC3B as well, but the interaction remains yet to be confirmed to be LIR-dependent.…”

Section: Unknown Specificitymentioning

confidence: 99%

Structure and Dynamics in the ATG8 Family From Experimental to Computational Techniques

Sora

Kumar

Maiani

et al. 2020

Front. Cell Dev. Biol.

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Autophagy is a conserved and essential intracellular mechanism for the removal of damaged components. Since autophagy deregulation is linked to different kinds of pathologies, it is fundamental to gain knowledge on the fine molecular and structural details related to the core proteins of the autophagy machinery. Among these, the family of human ATG8 proteins plays a central role in recruiting other proteins to the different membrane structures involved in the autophagic pathway. Several experimental structures are available for the members of the ATG8 family alone or in complex with their different biological partners, including disordered regions of proteins containing a short linear motif called LC3 interacting motif. Recently, the first structural details of the interaction of ATG8 proteins with biological membranes came into light. The availability of structural data for human ATG8 proteins has been paving the way for studies on their structure-function-dynamic relationship using biomolecular simulations. Experimental and computational structural biology can help to address several outstanding questions on the mechanism of human ATG8 proteins, including their specificity toward different interactors, their association with membranes, the heterogeneity of their conformational ensemble, and their regulation by post-translational modifications. We here summarize the main results collected so far and discuss the future perspectives within the field and the knowledge gaps. Our review can serve as a roadmap for future structural and dynamics studies of the ATG8 family members in health and disease.

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“…CSRP3 (Rashid et al, 2015) and FHL1 (Han et al, 2020) have been recently found to interact with LC3B as well, but the interaction remains yet to be confirmed to be LIR-dependent.…”

Section: Unknown Specificitymentioning

confidence: 99%

Structure and Dynamics in the ATG8 Family From Experimental to Computational Techniques

Sora

Kumar

Maiani

et al. 2020

Front. Cell Dev. Biol.

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“…Similarly, the overexpression of FHL1 increased myotube fusion and caused myotube hypertrophy in C2C12 cells, suggesting that FHL1 enhances skeletal myogenesis and muscle mass (19,20). On the other hand, Han et al recently reported that the knockdown of FHL1 decreased the myogenic markers, such as MyoD, MyoG, and MyHC, and reduced myotube formation in chicken primary myoblasts (24). In addition, the silencing of FHL1 increased Atrogin-1 and MuRF1, which led to muscle atrophy and wasting, unveiling the crucial roles of FHL1 in myogenic differentiation and maintenance (24).…”

Section: Discussionmentioning

confidence: 96%

MiR-183-5p induced by saturated fatty acids regulates the myogenic differentiation by directly targeting FHL1 in C2C12 myoblasts

2020

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Skeletal myogenesis is a complex process that is finely regulated by myogenic transcription factors. Recent studies have shown that saturated fatty acids (SFA) can suppress the activation of myogenic transcription factors and impair the myogenic differentiation of progenitor cells. Despite the increasing evidence of the roles of miRNAs in myogenesis, the targets and myogenic regulatory mechanisms of miRNAs are largely unknown, particularly when myogenesis is dysregulated by SFA deposition. This study examined the implications of SFA-induced miR-183-5p on the myogenic differentiation in C2C12 myoblasts. Long-chain SFA palmitic acid (PA) drastically reduced myogenic transcription factors, such as myoblast determination protein (MyoD), myogenin (MyoG), and myocyte enhancer factor 2C (MEF2C), and inhibited FHL1 expression and myogenic differentiation of C2C12 myoblasts, accompanied by the induction of miR-183-5p. The knockdown of FHL1 by siRNA inhibited myogenic differentiation of myoblasts. Interestingly, miR-183-5p inversely regulated the expression of FHL1, a crucial regulator of skeletal myogenesis, by targeting the 3'UTR of FHL1 mRNA. Furthermore, the transfection of miR-183-5p mimic suppressed the expression of MyoD, MyoG, MEF2C, and MyHC, and impaired the differentiation and myotube formation of myoblasts. Overall, this study highlights the role of miR-183-5p in myogenic differentiation through FHL1 repression and suggests a novel miRNA-mediated mechanism for myogenesis in a background of obesity. [BMB Reports 2020; 53(11): 605-610]

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“…The chicken primary myoblasts were extracted from the left breast muscle of embryonic day 11 Ross 308 broilers [13]. The primary myoblasts were cultured in the growth medium (GM), including Dulbecco's modified Eagle's medium (DMEM; Gibco, Grand Island, NY, USA), 0.5% penicillin/streptomycin (Sigma, St. Louis, MO, USA), and 15% fetal bovine serum (FBS; Gibco, Grand Island, NY, USA).…”

Section: Cell Culturesmentioning

confidence: 99%

Fibromodulin Modulates Chicken Skeletal Muscle Development via the Transforming Growth Factor-β Signaling Pathway

Yin

Cui

Han

et al. 2020

Animals

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Fibromodulin (Fmod), which is an extracellular matrix protein, belongs to the extracellular matrix small-leucine-rich proteoglycan family. Fmod is abundantly expressed in muscles and connective tissues and is involved in biological regulation processes, including cell apoptosis, cell adhesion, and modulation of cytokine activity. Fmod is the main regulator of myostatin, which controls the development of muscle cells, but its regulatory path is unknown. Chicken models are ideal for studying embryonic skeletal muscle development; therefore, to investigate the mechanism of Fmod in muscle development, Fmod-silenced and Fmod-overexpressed chicken myoblasts were constructed. The results showed that Fmod plays a positive role in differentiation by detecting the expression of myogenic differentiation markers, immunofluorescence of MyHC protein, and myotube formation in myoblasts. Fmod regulates expression of atrophy-related genes to alleviate muscle atrophy, which was confirmed by histological analysis of breast muscles in Fmod-modulated chicks in vivo. Additionally, genes differentially expressed between Fmod knockdown and normal myoblasts were enriched in the signaling pathway of transforming growth factor β (TGF-β). Both Fmod-silenced and Fmod-overexpressed myoblasts regulated the expression of TGFBR1 and p-Smad3. Thus, Fmod can promote differentiation but not proliferation of myoblasts by regulating the TGF-β signaling pathway, which may serve a function in muscular atrophy.

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FHL1 regulates myoblast differentiation and autophagy through its interaction with LC3

Cited by 24 publications

References 42 publications

Structure and Dynamics in the ATG8 Family From Experimental to Computational Techniques

Structure and Dynamics in the ATG8 Family From Experimental to Computational Techniques

MiR-183-5p induced by saturated fatty acids regulates the myogenic differentiation by directly targeting FHL1 in C2C12 myoblasts

Fibromodulin Modulates Chicken Skeletal Muscle Development via the Transforming Growth Factor-β Signaling Pathway

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