Bovine Milk Fat Globule Epidermal Growth Factor VIII activates PI3K/Akt signaling pathway and attenuates sarcopenia in rat model induced by d-galactose

Li, He; Wang, Rongchun; Wang, Lifeng; Li, Lin; Ma, Ying; Zhou, Shaobo

doi:10.1016/j.fbio.2020.100847

Cited by 9 publications

(4 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Sarcopenia is a chronic complication of T2DM, and currently no drugs are particularly effective. The present physiological and biochemical findings showed damaged gastrocnemius muscles and a significantly increased blood sugar level in our model rats with age-related T2DM and sarcopenia [22] . We investigated the effects of different doses of TDS on basic physiological indicators of the rats, namely body weight, body length, and final gastrocnemius muscle weight.…”

Section: Discussionmentioning

confidence: 66%

“…Gastrocnemius muscle samples were fixed in 10% formaldehyde, washed with sterile PBS, embedded in paraffin blocks, and cut into 5-μm-thick sections using a cryostat. The sections were loaded onto cationic slides and dried at 60°C for 1 h, deparaffinized, rehydrated, and stained with hematoxylin-eosin (HE) [22] . The stained sections were stored in darkness, incubated for 30 min in 36% triethyl phosphate with 3 mg/mL of Oil Red O [23] , rinsed three times with ddH 2 O, and covered with resin-bonded glass coverslips.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Campanumoea javanica Bl. activates the PI3K/AKT/mTOR signaling pathway and reduces sarcopenia in a T2DM rat model

Zuo

Yao

Zhao

et al. 2022

Acupuncture and Herbal Medicine

View full text Add to dashboard Cite

Objective: Sarcopenia causes loss of skeletal muscle and function, thus seriously affecting the physical function and quality of life in the elderly. This article discusses the specific molecular mechanism and ameliorating effects of Tudangshen (TDS) on sarcopenia in elderly rats with type 2 diabetes mellitus (T2DM).Methods: Elderly Sprague-Dawley (SD) rats were randomly selected and fed with a high-fat diet combined with an intraperitoneal injection of streptozotocin to establish T2DM model. The model rats were stratified and randomly divided into the model group, metformin group, TDS high-dose group, TDS medium-dose group, and TDS low-dose group according to blood glucose combined with body weight, and the same batch of old SD rats was set as the normal control group. The effects of TDS in an elderly T2DM sarcopenia rat model were evaluated by observing the body positions of the rats, analyzing blood biochemistry, testing exercise capacity, and pathologically staining sectioned gastrocnemius muscle tissues. The molecular mechanisms of the effects were analyzed using quantitative real-time polymerase chain reaction and western blotting.Results: TDS has no statistically significant effect on blood glucose, insulin and glycosylated serum protein in aged rats with T2DM, but it can reduce levels of glycosylated serum protein, total cholesterol, triglycerides, and low-density lipoprotein; it improves pathological changes in rat gastrocnemius muscle tissues, and increases muscle cell activity in elderly rats with T2DM and sarcopenia. TDS also promoted the upregulation of the expression of mammalian target of rapamycin (mTOR)/protein kinase B (PKB/AKT)/phosphatidylinositol 3-kinase (PI3K)/ribosomal protein S6 kinase/eukaryotic initiation factor 4E binding rotein1 mRNA in rats and triggered an increase in corresponding protein levels.Conclusions: TDS alleviated muscle decline in elderly rats with T2DM by activating the PI3K/AKT/mTOR signaling pathway and regulating the synthesis of corresponding proteins.

show abstract

Section: Discussionmentioning

confidence: 66%

Section: Methodsmentioning

confidence: 99%

Campanumoea javanica Bl. activates the PI3K/AKT/mTOR signaling pathway and reduces sarcopenia in a T2DM rat model

Zuo

Yao

Zhao

et al. 2022

Acupuncture and Herbal Medicine

View full text Add to dashboard Cite

show abstract

“…In support of our proposal, after submission of our manuscript, administration of MFG-E8 was reported to attenuate sarcopenia in a rat model induced by D-galactose. 102 What is more, a recent report, which investigated the key differentially expressed genes and pathways associated with the progression of sarcopenia, identified MFG-E8 as a significantly down-regulated gene in sarcopenic muscles and demonstrated that MFG-E8 has potential anti-sarcopenia effects by promoting extracellular signal-regulated kinase (ERK) and Akt activation-mediated cell proliferation and cell cycle progression in myoblasts. 103…”

Section: Discussionmentioning

confidence: 99%

Involvement of phosphatidylserine receptors in the skeletal muscle regeneration: therapeutic implications

Szondy

Al‐Zaeed

Tarban

et al. 2022

J cachexia sarcopenia muscle

View full text Add to dashboard Cite

Sarcopenia is a progressive loss of muscle mass and strength with a risk of adverse outcomes such as disability, poor quality of life, and death. Increasing evidence indicates that diminished ability of the muscle to activate satellite cell-dependent regeneration is one of the factors that might contribute to its development. Skeletal muscle regeneration following myogenic cell death results from the proliferation and differentiation of myogenic stem cells, called satellite cells, located beneath the basal lamina of the muscle fibres. Satellite cell differentiation is not a satellite cell-autonomous process but depends on signals provided by the surrounding cells. Infiltrating macrophages play a key role in the process partly by clearing the necrotic cell debris, partly by producing cytokines and growth factors that guide myogenesis. At the beginning of the muscle regeneration process, macrophages are pro-inflammatory, and the cytokines produced by them trigger the proliferation and differentiation of satellite cells. Following the uptake of dead cells, however, a transcriptionally regulated phenotypic change (macrophage polarization) is induced in them resulting in their transformation into healing macrophages that guide resolution of inflammation, completion of myoblast differentiation, myoblast fusion and growth, and return to homeostasis. Impaired efferocytosis results in delayed cell death clearance, delayed macrophage polarization, prolonged inflammation, and impaired muscle regeneration. Thus, proper efferocytosis by macrophages is a determining factor during muscle repair. Here we review that both efferocytosis and myogenesis are dependent on the cell surface phosphatidylserine (PS), and surprisingly, these two processes share a number of common PS receptors and signalling pathways. Based on these findings, we propose that stimulating the function of PS receptors for facilitating muscle repair following injury could be a successful approach, as it would enhance efferocytosis and myogenesis simultaneously. Because increasing evidence indicates a pathophysiological role of impaired efferocytosis in the development of chronic inflammatory conditions, as well as in impaired muscle regeneration both contributing to the development of sarcopenia, improving efferocytosis should be considered also in its management. Again applying or combining those treatments that target PS receptors would be expected to be the most effective, because they would also promote myogenesis. A potential PS receptor-triggering candidate molecule is milk fat globule-EGF-factor 8 (MFG-E8), which not only stimulates PS-dependent efferocytosis and myoblast fusion but also promotes extracellular signal-regulated kinase (ERK) and Akt activation-mediated cell proliferation and cell cycle progression in myoblasts.

show abstract

“…Thus, DHM may be beneficial for the treatment of skeletal muscle atrophy and its prevention during the aging process. In addition, by using a D-gal-induced sarcopenia rat model, Li et al revealed that bovine milk fat globule epidermal growth factor VIII inhibits cell apoptosis in the gastrocnemius muscle to prevent muscle mass loss [ 112 ].…”

Section: Rodent Models For Skeletal Muscle Senescencementioning

confidence: 99%

Zebrafish Models for Skeletal Muscle Senescence: Lessons from Cell Cultures and Rodent Models

2022

View full text Add to dashboard Cite

Human life expectancy has markedly increased over the past hundred years. Consequently, the percentage of elderly people is increasing. Aging and sarcopenic changes in skeletal muscles not only reduce locomotor activities in elderly people but also increase the chance of trauma, such as bone fractures, and the incidence of other diseases, such as metabolic syndrome, due to reduced physical activity. Exercise therapy is currently the only treatment and prevention approach for skeletal muscle aging. In this review, we aimed to summarize the strategies for modeling skeletal muscle senescence in cell cultures and rodents and provide future perspectives based on zebrafish models. In cell cultures, in addition to myoblast proliferation and myotube differentiation, senescence induction into differentiated myotubes is also promising. In rodents, several models have been reported that reflect the skeletal muscle aging phenotype or parts of it, including the accelerated aging models. Although there are fewer models of skeletal muscle aging in zebrafish than in mice, various models have been reported in recent years with the development of CRISPR/Cas9 technology, and further advancements in the field using zebrafish models are expected in the future.

show abstract

Bovine Milk Fat Globule Epidermal Growth Factor VIII activates PI3K/Akt signaling pathway and attenuates sarcopenia in rat model induced by d-galactose

Cited by 9 publications

References 43 publications

Campanumoea javanica Bl. activates the PI3K/AKT/mTOR signaling pathway and reduces sarcopenia in a T2DM rat model

Campanumoea javanica Bl. activates the PI3K/AKT/mTOR signaling pathway and reduces sarcopenia in a T2DM rat model

Involvement of phosphatidylserine receptors in the skeletal muscle regeneration: therapeutic implications

Zebrafish Models for Skeletal Muscle Senescence: Lessons from Cell Cultures and Rodent Models

Contact Info

Product

Resources

About