Ginsenoside compound K ameliorates palmitate-induced atrophy in C2C12 myotubes via promyogenic effects and AMPK/autophagy-mediated suppression of endoplasmic reticulum stress

Kim, Tae Jin; Pyun, Do Hyeon; Kim, Myeong Jun; Jeong, Ji Hoon; El‐Aty, A.M. Abd; Jung, Tae Woo

doi:10.1016/j.jgr.2021.09.002

Cited by 19 publications

(10 citation statements)

References 52 publications

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“…To investigate the function of Kcnma1 in myoblast viability under DM condition, cells were infected with the Kcnma1 ‐modified recombinant adenoviruses for 48 h and then treated with 250 μM of palmitate (Macklin Inc., Shanghai, China) for 16 h. As the most abundant free fatty acid, palmitate accounts for about 30% of total free fatty acids in human plasma, and its increase is closely related to DM progression 17 . According to a previous report, treatment of C2C12 myotubes with palmitate reduced the myotube thickness and enhanced cell apoptosis, along with changes in myogenesis markers 18 …”

Section: Methodsmentioning

confidence: 99%

“…17 According to a previous report, treatment of C2C12 myotubes with palmitate reduced the myotube thickness and enhanced cell apoptosis, along with changes in myogenesis markers. 18 To induce myogenic differentiation, cells grown at a 95% confluence were cultured with differentiation medium (DMEM and 2% horse serum; Solarbio) for 5 days, then subjected to western blot or flow cytometry for detection of myogenesis and mitochondrial function.…”

Section: Cell Culture and Adenoviral Infectionmentioning

confidence: 99%

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Kcnma1 is involved in mitochondrial homeostasis in diabetes‐related skeletal muscle atrophy

et al. 2023

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Uncontrolled diabetes causes a catabolic state with multi-organic complications, of which impairment on skeletal muscle contributes to the damaged mobility. Kcnma1 gene encodes the pore-forming αsubunit of Ca 2+ -and voltage-gated K + channels of large conductance (BK channels), and loss-of-function mutations in Kcnma1 are in regards to impaired myogenesis. Herein, we observed a timecourse reduction of Kcnma1 expression in the tibialis anterior muscles of leptin receptor-deficient (db/db) diabetic mice. To investigate the role of Kcnma1 in diabetic muscle atrophy, muscle-specific knockdown of Kcnma1 was achieved by mice receiving intravenous injection of adeno-associated virus-9 (AAV9)encoding shRNA against Kcnma1 under the muscle creatine kinase (MCK) promoter. Impairment on muscle mass and myogenesis were observed in m/m mice with AAV9-shKcnma1 intervention, while this impairment was more obvious in diabetic db/db mice. Simultaneously, damaged mitochondrial dynamics and biogenesis showed much severer in db/db mice with AAV9-shKcnma1 intervention. RNA sequencing revealed the large transcriptomic changes resulted by Kcnma1 knockdown, and changes in mitochondrial homeostasis-related genes were validated. Besides, the artificial alteration of Kcnma1 in mouse C2C12 myoblasts was achieved with an adenovirus vector. Consistent results were demonstrated How to cite this article: Gao S-Y, Liu Y-P, Wen R, et al. Kcnma1 is involved in mitochondrial homeostasis in diabetes-related skeletal muscle atrophy.

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Section: Methodsmentioning

confidence: 99%

Section: Cell Culture and Adenoviral Infectionmentioning

confidence: 99%

Kcnma1 is involved in mitochondrial homeostasis in diabetes‐related skeletal muscle atrophy

et al. 2023

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“…A previous study showed that palmitate treatment negatively affects myotube differentiation and promotes proteolytic signaling (Yang et al, 2013). Palmitate shows lipotoxicity in muscle cells via induction of insulin resistance (Chavez & Summers, 2003), autophagy (Kim et al, 2022), mitochondrial dysfunction, and endoplasmic reticulum stress (Eo & Valentine, 2022), leading to cellular damage and cell death (Zhang et al, 2022); this indicates that palmitate treatment can be used to generate a model of type 2 diabetes. Skeletal muscle is an important tissue for insulin‐stimulated glucose consumption.…”

Section: Introductionmentioning

confidence: 99%

A lipidomics approach reveals novel phospholipid changes in palmitate‐treated C2C12 myotubes

Tawara,

Morisasa,

Mukai

et al. 2024

Lipids

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Type 2 diabetes mellitus (T2DM) is a highly prevalent metabolic disorder. Insulin resistance and oxidative stress are associated with T2DM development. The hypothesis that patients with T2DM show excess accumulation of lipids, such as ceramides (Cers) and diacylglycerols (DAGs), in their skeletal muscles has been widely supported; however, detailed lipidomic data at the molecular species level are limited. Therefore, in this study, we aimed to investigate the in vitro dynamics of total lipids, including phospholipids (PLs), sphingolipids, and neutral lipids, in palmitic acid‐induced insulin‐resistant C2C12 skeletal muscle cells. Our data demonstrated that the profiles of not only Cers and DAGs but also those of PLs showed considerably differences after palmitate treatment. We found that PL synthesis reduced and PL degradation increased after palmitate treatment. These findings may aid in the development of treatments to ameliorate muscle dysfunction caused by lipid accumulation in muscles.

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“…CK can inhibit thioredoxin interacting protein (TXNIP) that can be activated by IRE1α to subsequently activate the NLRP3 inflammasome in adipose tissues and myoblasts. − IRE1α activation has been shown to contribute to OA pathogenesis . However, the interaction of ERS with inflammation and cell pyroptosis via TXNIP in OA and the effect of CK on this process are unclear.…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside Compound K Ameliorates Osteoarthritis by Inhibiting the Chondrocyte Endoplasmic Reticulum Stress-Mediated IRE1α-TXNIP-NLRP3 Axis and Pyroptosis

You

Feng

Zhou

et al. 2023

J. Agric. Food Chem.

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Osteoarthritis (OA) is a common joint disease, and studies have reported that the endoplasmic reticulum stress (ERS) in chondrocytes caused by the cartilage tissue damage could mediate the activation of Nod-like receptor protein 3 (NLRP3) inflammasomes through inositol-requiring enzyme 1 alpha (IRE1α) and thioredoxin interacting protein (TXNIP). Ginsenoside compound K (CK) has an inhibitory effect on IRE1α activation. However, the role of IRE1α-TXNIP and its interaction with CK are still unclear. In this study, we examined the role and mechanism of action of CK in OA. We found that CK ameliorated OA and ERS in IL-1β-treated chondrocytes and a monoiodoacetate-induced rat OA model. The effect of CK on inflammation, pyroptosis, and ERS was blocked by the ERS inducer tunicamycin. In conclusion, CK hindered OA progression by inhibiting the ERS-IRE1α-TXNIP-NLRP3 axis. Overall, our data indicate that CK could be useful in the treatment of OA and other chronic inflammatory diseases.

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Ginsenoside compound K ameliorates palmitate-induced atrophy in C2C12 myotubes via promyogenic effects and AMPK/autophagy-mediated suppression of endoplasmic reticulum stress

Cited by 19 publications

References 52 publications

Kcnma1 is involved in mitochondrial homeostasis in diabetes‐related skeletal muscle atrophy

Kcnma1 is involved in mitochondrial homeostasis in diabetes‐related skeletal muscle atrophy

A lipidomics approach reveals novel phospholipid changes in palmitate‐treated C2C12 myotubes

Ginsenoside Compound K Ameliorates Osteoarthritis by Inhibiting the Chondrocyte Endoplasmic Reticulum Stress-Mediated IRE1α-TXNIP-NLRP3 Axis and Pyroptosis

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