Dedifferentiation, Redifferentiation, and Transdifferentiation of Striated Muscles During Regeneration and Development

Frasch, Manfred

doi:10.1016/bs.ctdb.2015.12.005

Cited by 19 publications

(12 citation statements)

References 79 publications

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“…However, myotubes at the end stage of differentiation cannot transform into adipocytes [2]. Some studies have focused on molecular characterization and regulatory mechanisms underlying transformation between muscle and fat cells, and data show that trans-differentiation is complex involving reprogramming of many genes and cell fate changes [7, 8]. …”

Section: Introductionmentioning

confidence: 99%

Expressions and Regulatory Effects of P38/ERK/JNK Mapks in the Adipogenic Trans-Differentiation of C2C12 Myoblasts

Qi¹,

Wang³

et al. 2017

Cell Physiol Biochem

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Background/Aims: Myoblasts and muscle satellite cells have the potential to transdifferentiate into adipocytes or adipocyte-like cells. Previous studies suggest that mitogen-activated protein kinase (MAPK) is critical to adipogenic trans-differentiation of muscle cells. ERK1/2, P38 and JNK are three major MAPK family members; their activation and regulatory functions during adipogenic trans-differentiation of myoblasts are investigated. Methods: C2C12 myoblasts were cultured and induced for adipogenic trans-differentiation. Activation patterns of MAPKs were assayed using protein microarray and Western blot. Three specific MAPK blockers, U0126, SB20358 and SP600125, were used to block ERK1/2, P38 and JNK during trans-differentiation. Cellular adipogenesis was measured using staining and morphological observations of cells and expression changes in adipogenic genes. Results: Inhibitors reduced phosphorylation of corresponding MAPK and produced unique cellular effects. Suppressing P38 promoted adipogenic trans-differentiation and intensified adipolytic metabolism in differentiated cells. However, inhibition of ERK1/2 had the opposite effects on adipogenesis and no effect on adipolysis. Blocking JNK weakly blocked trans-differentiation but stimulated adipolysis and induced apoptosis. Conclusion: Three MAPKs participate in the regulation of myoblast adipogenic trans-differentiation by controlling adipogenic and adipolysis metabolism.

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Section: Introductionmentioning

confidence: 99%

Expressions and Regulatory Effects of P38/ERK/JNK Mapks in the Adipogenic Trans-Differentiation of C2C12 Myoblasts

Qi¹,

Wang³

et al. 2017

Cell Physiol Biochem

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“…Although syncytial muscles are often considered a paragon of terminally differentiated cells there are rare examples where skeletal muscle cells are induced to dedifferentiate and fragment into muscle progenitor cells, either by forced treatment or during a natural process as for the anterior Drosophila alary muscles [2, 17]. Our results herein reveal that effectors of the JNK and Hpo signaling pathways drive the lineage specific dedifferentiation and fragmentation of syncytial AM cells into mononucleate myoblasts.…”

Section: Resultsmentioning

confidence: 65%

Yorkie and JNK revert syncytial muscles into myoblasts during Org-1 dependent lineage reprogramming

Schaub

Rose

Frasch

2019

Preprint

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SummaryLineage reprogramming has become a prominent focus in research since it was demonstrated that lineage restricted transcription factors can be used in vitro for direct reprogramming [1]. Recently, we reported that the ventral longitudinal musculature (VLM) of the adult Drosophila heart arises in vivo by direct lineage reprogramming from alary muscles (AM), a process which starts with dedifferentiation and fragmentation of syncytial alary muscles into mononucleate myoblasts. Central upstream activators of the genetic program regulating the development of VLMs from alary muscles are the T-box factor Org-1 (Drosophila Tbx1) and the LIM homeodomain factor Tup (Drosophila Islet1) [2]. However, the events downstream of Org-1 and Tup that exert dedifferentiation and fragmentation of alary muscles have been unknown. In the present report, we shed light on the initiation of this first step of transdifferentiation and show that AM lineage specific activation of Yorkie (Yki), the transcriptional co-activator of the transcription factor Scalloped (Sd), has a key role in initiating AM lineage reprogramming. An additional necessary input comes from active dJNK signaling, which contributes to the inactivation of the Hippo kinase cascade upstream of Yki and furthermore activates dJun. The synergistic activities of the Yki/Sd and dJun/dFos (AP-1) transcriptional activator complexes in the absence of Hippo activity initiate AM dedifferentiation and lead to the expression of Myc and piwi, which are crucial for different aspects of AM transdifferentiation. Our results provide new insights into the mechanisms that mediate muscle lineage plasticity during a cellular reprogramming process occurring in vivo.HighlightsDirect lineage reprogramming of alary muscles depends on Yorkie and JNKYorkie and JNK mediate reversal of syncytial muscle cell fateYki/Sd and AP-1 induce alary muscle dedifferentiation synergisticallyYki dependent Myc induces and Piwi mediates reprogramming of alary muscles

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“…In recent years, we have gained new insights into the adipogenesis in muscle cells. To our knowledge, the formation of muscle, bone, and adipose tissues involves a multistep processes that includes the determination of a common progenitor mesodermal cell toward a specific differentiation pathway, followed by the expression of various terminal differentiation phenotypes [34]. In vitro studies have demonstrated the multi-directional differentiation potential of muscle-derived stem cells or precursor cells [1,2,3,4,5,6,35,36].…”

Section: Discussionmentioning

confidence: 99%

Comparison of LncRNA Expression Profiles during Myogenic Differentiation and Adipogenic Transdifferentiation of Myoblasts

Qiu²,

Zhang

et al. 2019

IJMS

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Myoblasts could transdifferentiate into adipocytes or adipocyte-like cells, which have the capability of producing and storing intracellular lipids. Long-chain non-coding RNAs (lncRNAs) have many important physiological functions in eukaryotes, which include regulating gene expression, chromosome silencing, and nuclear transport. However, changes in the expression of lncRNAs in muscle cells during adipogenic transdifferentiation have not been investigated to date. Here, C2C12 myoblasts were seeded and then induced to undergo myogenic and adipogenic transdifferentiation. The expression profiles of lncRNAs in various differentiated cells were analyzed and then compared by digital gene expression (DGE) RNA sequencing. A total of 114 core lncRNAs from 836 differentially expressed lncRNAs in adipogenic cells were identified. Further investigation by in silico analysis revealed that the target genes of core lncRNAs significantly enriched various signaling pathways that were related to glucose and lipid metabolism and muscle growth. The lncRNA-GM43652 gene was a potential regulator of adipogenesis in muscle cells. It showed the highest levels of expression in adipogenic cells, and the knocking down lncRNA-GM43652 negatively influenced lipid deposition in transdifferentiated myoblasts. This study has identified the novel candidate regulators that may be assessed in future molecular studies on adipogenic conversion of muscle cells.

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Dedifferentiation, Redifferentiation, and Transdifferentiation of Striated Muscles During Regeneration and Development

Cited by 19 publications

References 79 publications

Expressions and Regulatory Effects of P38/ERK/JNK Mapks in the Adipogenic Trans-Differentiation of C2C12 Myoblasts

Expressions and Regulatory Effects of P38/ERK/JNK Mapks in the Adipogenic Trans-Differentiation of C2C12 Myoblasts

Yorkie and JNK revert syncytial muscles into myoblasts during Org-1 dependent lineage reprogramming

Comparison of LncRNA Expression Profiles during Myogenic Differentiation and Adipogenic Transdifferentiation of Myoblasts

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