The Crosstalk between Autophagy and Apoptosis Is Necessary for Myogenic Differentiation

Jiang, Aiwen; Guo, Hongyun; Wu, Wangjun; Liu, Honglin

doi:10.1021/acs.jafc.1c00140

Cited by 16 publications

(20 citation statements)

References 34 publications

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“…Autophagy and apoptosis coexist in early muscle injury throughout regeneration because the former is responsible for cell reprogramming by regulating cytoplasmic remodelling, while the latter eliminates defective cells that do not have differentiation potential [ 49 , 50 ]. The crosstalk between apoptosis and autophagy determines the balance of cell survival and death, allowing SCs to differentiate normally [ 51 ]. However, improper autophagy and apoptosis hamper myotube formation and muscle regeneration [ 52 , 53 ].…”

Section: Discussionmentioning

confidence: 99%

Selenoprotein K protects skeletal muscle from damage and is required for satellite cells-mediated myogenic differentiation

et al. 2022

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Section: Discussionmentioning

confidence: 99%

Selenoprotein K protects skeletal muscle from damage and is required for satellite cells-mediated myogenic differentiation

et al. 2022

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“…Double immunofluorescence staining for CDK5RAP3 and calnexin (a calcium‐binding protein located on the endoplasmic reticulum membrane) showed that part of the CDK5RAP3 protein was located in the endoplasmic reticulum (Figure S3A). There are multiple inseparable links between apoptosis and autophagy 40,41 . Lyso‐Tracker Red was used to stain lysosomes in living cells.…”

Section: Resultsmentioning

confidence: 99%

“…There are multiple inseparable links between apoptosis and autophagy. 40,41 Lyso-Tracker Red was used to stain lysosomes in living cells. As results shown in Figure 7A, CDK5RAP3 deficiency forced the fluorescence brightness to increase, and it is more concentrated around the cytoplasm near the nucleus compared with the EtOH group (lysosomes are evenly distributed in the cytoplasm).…”

Section: Cdk5rap3 Deficiency Regulated Mtor Pathway and Lead Autophagymentioning

confidence: 99%

CDK5RAP3, an essential regulator of checkpoint, interacts with RPL26 and maintains the stability of cell growth

Yan

Ali

et al. 2022

Cell Proliferation

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Purpose and Materials: CDK5RAP3 (CDK5 regulatory subunit associated protein 3) was originally identified as a binding protein of CDK5. It is a crucial gene controlling biological functions, such as cell proliferation, apoptosis, invasion, and metastasis.Although previous studies have also shown that CDK5RAP3 is involved in a variety of signalling pathways, however, the mechanism of CDK5RAP3 remains largely undefined. This study utilized MEFs from conditional knockout mice to inhibit CDK5RAP3 and knockdown CDK5RAP3 in MCF7 to explore the role of CDK5RAP3 in cell growth, mitosis, and cell death.Results: CDK5RAP3 was found to be widely distributed throughout the centrosome, spindle, and endoplasmic reticulum, indicating that it is involved in regulating a variety of cellular activities. CDK5RAP3 deficiency resulted in instability of cell growth.CDK5RAP3 deficiency partly blocks the cell cycle in G 2 /M by downregulating CDK1 (Cyclin-dependent kinase 1) and CCNB1 (Cyclin B1) expression levels. The cell proliferation rate was decreased, thereby slowing down the cell growth rate. Furthermore, the results showed that CDK5RAP3 interacts with RPL26 (ribosome protein L26) to regulate the mTOR pathway. CDK5RAP3 and RPL26 deficiency inhibited mTOR/p-mTOR protein and induce autophagy, resulting in an upregulation of the percentage of apoptosis, and the upregulated percentage of apoptosis also slowed cell growth. Conclusions:Our experiments show that CDK5RAP3 interacts with RPL26 and maintains the stability of cell growth. It shows that CDK5RAP3 plays an important role in cell growth and can be used as the target of gene medicine.

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“…The crosstalk between apoptosis and autophagy is important in cellular metabolic survival and cellular housekeeping mechanisms [ 46 , 47 , 48 ]. It has been reported that modulating the autophagy of osteoblasts could avoid oxidative damage and allow cells to continue normal function through the endoplasmic reticulum stress pathway [ 49 ].…”

Section: Discussionmentioning

confidence: 99%

Ablation of Discoidin Domain Receptor 1 Provokes an Osteopenic Phenotype by Regulating Osteoblast/Osteocyte Autophagy and Apoptosis

et al. 2022

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Discoidin domain receptor 1 (DDR1) is a collagen receptor that belongs to the receptor tyrosine kinase family. We have previously shown that DDR1 plays a crucial role during bone development, resulting in dwarfism and a short stature in osteoblast-specific knockout mice (OKO mice). However, the detailed pathophysiological effects of DDR1 on bone development throughout adulthood have remained unclear. This study aims to identify how DDR1 regulates osteoblast and osteocyte functions in vivo and in vitro during bone development in adulthood. The metabolic changes in bone tissues were analyzed using Micro-CT and immunohistochemistry staining (IHC) in vivo; the role of DDR1 in regulating osteoblasts was examined in MC3T3-E1 cells in vitro. The Micro-CT analysis results demonstrated that OKO mice showed a 10% reduction in bone-related parameters from 10 to 14 weeks old and a significant reduction in cortical thickness and diameter compared with flox/flox control mice (FF) mice. These results indicated that DDR1 knockout in OKO mice exhibiting significant bone loss provokes an osteopenic phenotype. The IHC staining revealed a significant decrease in osteogenesis-related genes, including RUNX2, osteocalcin, and osterix. We noted that DDR1 knockout significantly induced osteoblast/osteocyte apoptosis and markedly decreased autophagy activity in vivo. Additionally, the results of the gain- and loss-of-function of the DDR1 assay in MC3T3-E1 cells indicated that DDR1 can regulate the osteoblast differentiation through activating autophagy by regulating the phosphorylation of the mechanistic target of rapamycin (p-mTOR), light chain 3 (LC3), and beclin-1. In conclusion, our study highlights that the ablation of DDR1 results in cancellous bone loss by regulating osteoblast/osteocyte autophagy. These results suggest that DDR1 can act as a potential therapeutic target for managing cancellous bone loss.

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The Crosstalk between Autophagy and Apoptosis Is Necessary for Myogenic Differentiation

Cited by 16 publications

References 34 publications

Selenoprotein K protects skeletal muscle from damage and is required for satellite cells-mediated myogenic differentiation

Selenoprotein K protects skeletal muscle from damage and is required for satellite cells-mediated myogenic differentiation

CDK5RAP3, an essential regulator of checkpoint, interacts with RPL26 and maintains the stability of cell growth

Ablation of Discoidin Domain Receptor 1 Provokes an Osteopenic Phenotype by Regulating Osteoblast/Osteocyte Autophagy and Apoptosis

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