Sestrin2 protects against bavachin induced ER stress through AMPK/mTORC1 signaling pathway in HepG2 cells

Yang, Ying; Guo, Guiming; Zhou, Wei; Ge, Yunxuan; Fan, Zheng; Liu, Qingquan; Gao, Yue

doi:10.1016/j.jphs.2020.11.012

Cited by 22 publications

(24 citation statements)

References 33 publications

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“…Life 2021, 11, 1408 9 of 11 ER stress plays a major role in cardiac myopathies. Activation of AMPK was shown to inhibit ER stress in previous studies [19,20]. Ezetimibe, a cholesterol absorption inhibitor, was shown to reduce IR-induced oxidative stress and UPR pathway activation through activation of AMPK [22].…”

Section: Discussionmentioning

confidence: 92%

“…Activation of PPARδ by PPARδ agonists in human umbilical cord vein cells (HUVECs) was found to attenuate ER stress induced by the plasma from patients with lupus nephritis [18]. Activation of AMPK was also shown to inhibit ER stress in previous studies [19,20]. We attempted to identify the relationship among HR, ER stress, PPARδ, and AMPK in this study.…”

Section: The Effect Of Adenine On Ampk and Pparδ Expressionmentioning

confidence: 97%

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The Cell Protective Effect of Adenine on Hypoxia–Reoxygenation Injury through PPAR Delta Activation

Leu

Wang

Chen

et al. 2021

Life

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Ischemia followed by blood supply reperfusion in cardiomyocytes leads to an overproduction of free radicals and a rapid decrease of adenosine triphosphate concentration. The cardioprotective effect of a potential drug, adenine, was evaluated using H9c2 rat cardiomyoblasts. After hypoxia–reoxygenation (HR) treatment consisting of hypoxia for 21 h followed by reoxygenation for 6 h, it was revealed that pretreatment with 200 µM adenine for 2 h effectively prevented HR-induced cell death. Adenine also significantly decreased the production of reactive oxygen species and reduced cell apoptosis after HR injury. The antioxidant effect of adenine was also revealed in this study. Adenine pretreatment significantly reduced the expression of activating transcription factor 4 (ATF4) and glucose-regulated protein 78 (GRP78) proteins, and protein disulfide isomerase induced a protective effect on mitochondria after HR stimulation. Intracellular adenosine monophosphate-activated protein kinase, peroxisome proliferator-activated receptor delta (PPARδ), and perilipin levels were increased by adenine after HR stimulation. Adenine had a protective effect in HR-damaged H9c2 cells. It may be used in multiple preventive medicines in the future.

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Section: Discussionmentioning

confidence: 92%

Section: The Effect Of Adenine On Ampk and Pparδ Expressionmentioning

confidence: 97%

The Cell Protective Effect of Adenine on Hypoxia–Reoxygenation Injury through PPAR Delta Activation

Leu

Wang

Chen

et al. 2021

Life

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“…In the absence of SESN2, cells are highly susceptible to ER-related pathologies, including mitochondrial dysfunction, lipid accumulation, protein aggregate formation, and apoptosis [ 72 – 74 ]. SESN2 acts as a crucial regulator in ER stress-related atherosclerosis [ 75 ], liver injury [ 76 , 77 ], spinal cord injury [ 78 ], and sepsis-related dendritic cell apoptosis [ 79 ]. The AMPK/mTORC1 pathway, CCAAT-enhancer-binding protein homologous protein, phosphorylation of both p38 and JNK, and sestrin-mediated unfolded protein response contribute to the protective mechanisms of SESN2 against ER stress-associated diseases [ 72 , 75 – 77 ].…”

Section: Biological Functions Of Sesns In Human Pathophysiological Processesmentioning

confidence: 99%

“…SESN2 protected macrophages from apoptosis and alleviated the excessive inflammatory response of macrophages in diseases such as myocardial infarction [ 91 – 93 ]. Monocytes can also be regulated by Sesn2 to reduce the damage caused by LPS-induced inflammation, atherosclerosis, high-glucose status, high-fat condition, and sepsis [ 76 , 84 , 94 ]. Mechanically, SESN2 knockdown significantly increases the secretion of pro-inflammatory cytokines, regulates monocyte polarization, and increases monocyte recruitment to the vascular endothelial cells by downregulating AMPK signaling and the ER stress pathway.…”

Section: Biological Functions Of Sesns In Human Pathophysiological Processesmentioning

confidence: 99%

The functions and roles of sestrins in regulating human diseases

Chen

Huang

et al. 2022

Cell Mol Biol Lett

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Sestrins (Sesns), highly conserved stress-inducible metabolic proteins, are known to protect organisms against various noxious stimuli including DNA damage, oxidative stress, starvation, endoplasmic reticulum (ER) stress, and hypoxia. Sesns regulate metabolism mainly through activation of the key energy sensor AMP-dependent protein kinase (AMPK) and inhibition of mammalian target of rapamycin complex 1 (mTORC1). Sesns also play pivotal roles in autophagy activation and apoptosis inhibition in normal cells, while conversely promoting apoptosis in cancer cells. The functions of Sesns in diseases such as metabolic disorders, neurodegenerative diseases, cardiovascular diseases, and cancer have been broadly investigated in the past decades. However, there is a limited number of reviews that have summarized the functions of Sesns in the pathophysiological processes of human diseases, especially musculoskeletal system diseases. One aim of this review is to discuss the biological functions of Sesns in the pathophysiological process and phenotype of diseases. More significantly, we include some new evidence about the musculoskeletal system. Another purpose is to explore whether Sesns could be potential biomarkers or targets in the future diagnostic and therapeutic process.

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“…ER stress is involved in various biological processes of cancer and is closely related to biological functions, such as proliferation, apoptosis, drug resistance, and autophagy [ 90 – 92 ]. Sestrin 2 expression is upregulated under ER stress in cancer cells through the regulation of the activating transcription factor 4 [ 93 ], inositol-requiring enzyme 1/X-box binding protein 1, and protein kinase RNA-like endoplasmic reticulum kinase signaling pathways [ 87 , 94 ]. Sestrin 2 knockdown reduced ER stress-induced autophagy and promoted ER stress-induced cell death by activating the mTORC1 pathway in breast cancer cells lines HCC1806 and MCF7 [ 87 ].…”

Section: Promotive Effects Of Sestrin 2 In Cancermentioning

confidence: 99%

A paradoxical role for sestrin 2 protein in tumor suppression and tumorigenesis

Luo

Zhang

et al. 2021

Cancer Cell Int

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Sestrin 2, a highly conserved stress-induced protein, participates in the pathological processes of metabolic and age-related diseases. This p53-inducible protein also regulates cell growth and metabolism, which is closely related to malignant tumorigenesis. Sestrin 2 was reported to regulate various cellular processes, such as tumor cell proliferation, invasion and metastasis, apoptosis, anoikis resistance, and drug resistance. Although sestrin 2 is associated with colorectal, lung, liver, and other cancers, sestrin 2 expression varies among different types of cancer, and the effects and mechanisms of action of this protein are also different. Sestrin 2 was considered a tumor suppressor gene in most studies, whereas conflicting reports considered sestrin 2 an oncogene. Thus, this review aims to examine the literature regarding sestrin 2 in various cancers, summarize its roles in suppression and tumorigenesis, discuss potential mechanisms in the regulation of cancer, and provide a basis for follow-up research and potential cancer treatment development.

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Sestrin2 protects against bavachin induced ER stress through AMPK/mTORC1 signaling pathway in HepG2 cells

Cited by 22 publications

References 33 publications

The Cell Protective Effect of Adenine on Hypoxia–Reoxygenation Injury through PPAR Delta Activation

The Cell Protective Effect of Adenine on Hypoxia–Reoxygenation Injury through PPAR Delta Activation

The functions and roles of sestrins in regulating human diseases

A paradoxical role for sestrin 2 protein in tumor suppression and tumorigenesis

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