Targeting the miR-122/PKM2 autophagy axis relieves arsenic stress

Wang, Yu; Zhao, Hongjing; Guo, Menghao; Fei, Dongxue; Zhang, Lina; Xing, Mingwei

doi:10.1016/j.jhazmat.2019.121217

Cited by 93 publications

(35 citation statements)

References 55 publications

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“…Our previous study had shown that G-CSF can upregulate the decreased microRNA-122 expressions in the dorsal root ganglia at the early phase after nerve injury, then the upregulated microRNA-122 can suppress monocyte chemoattractant protein-1 (MCP-1) expressions, which further attenuate neuropathic pain [ 5 ]. Wang’s study has shown that microRNA-122 can promote autophagic activities in the hepatocytes under arsenic stress [ 66 ]. Thus, G-CSF treatment probably also upregulated autophagic activities through upregulating microRNA-122 levels.…”

Section: Discussionmentioning

confidence: 99%

Interactions between Autophagy, Proinflammatory Cytokines, and Apoptosis in Neuropathic Pain: Granulocyte Colony Stimulating Factor as a Multipotent Therapy in Rats with Chronic Constriction Injury

Liao

Yeh

et al. 2021

Biomedicines

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Our previous studies have shown that early systemic granulocyte colony-stimulating factor (G-CSF) treatment can attenuate neuropathic pain in rats with chronic constriction injury (CCI) by modulating expression of different proinflammatory cytokines, microRNAs, and proteins. Besides the modulation of inflammatory mediators’ expression, previous studies have also reported that G-CSF can modulate autophagic and apoptotic activity. Furthermore, both autophagy and apoptosis play important roles in chronic pain modulation. In this study, we evaluated the temporal interactions of autophagy, and apoptosis in the dorsal root ganglion (DRG) and injured sciatic nerve after G-CSF treatment in CCI rats. We studied the behaviors of CCI rats with or without G-CSF treatment and the various levels of autophagic, proinflammatory, and apoptotic proteins in injured sciatic nerves and DRG neurons at different time points using Western blot analysis and immunohistochemical methods. The results showed that G-CSF treatment upregulated autophagic protein expression in the early phase and suppressed apoptotic protein expression in the late phase after nerve injury. Thus, medication such as G-CSF can modulate autophagy, apoptosis, and different proinflammatory proteins in the injured sciatic nerve and DRG neurons, which have the potential to treat neuropathic pain. However, autophagy-mediated regulation of neuropathic pain is a time-dependent process. An increase in autophagic activity in the early phase before proinflammatory cytokines reach the threshold level to induce neuropathic pain can effectively alleviate further neuropathic pain development.

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Section: Discussionmentioning

confidence: 99%

Interactions between Autophagy, Proinflammatory Cytokines, and Apoptosis in Neuropathic Pain: Granulocyte Colony Stimulating Factor as a Multipotent Therapy in Rats with Chronic Constriction Injury

Liao

Yeh

et al. 2021

Biomedicines

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“…Inflammation and deposition of oxidation products is one of the major causes of cardiovascular disease. miRNAs can participate in a variety of physiological and pathological responses in the organism (Y. Wang et al, 2020). Se can participate in the regulation of various functions of the organism through miRNAs.…”

Section: Discussionmentioning

confidence: 99%

“…Mature miRNAs are produced by longer primary transcripts undergoing a series of nuclease cutting processes, which are then assembled into RNA‐induced silencing complexes, and target messenger RNAs (mRNAs) are identified by complementary base pairing, and based on complementarity, different guidance‐silencing complexes degrade target mRNA or suppress translation of target mRNA. It plays an important regulatory role in various physiological processes in the organism (Y. Wang et al, 2020). MiRNAs are widely involved in cell proliferation (Chen et al, 2006), differentiation (Hinton et al, 2012), apoptosis (X. Wang et al, 2017; Welch et al, 2007), and physiological or pathological processes, such as organism development (Alvarez‐Garcia & Miska, 2005), metabolism (Boehm & Slack, 2006), and tumor formation.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‐223 triggers inflammation in porcine aorta by activating NLRP3 inflammasome under selenium deficiency

Zhang

Han

et al. 2020

Journal Cellular Physiology

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Selenium (Se) is an essential trace element in organism. Se deficiency can cause many diseases, including vascular disease. Studies have shown that inflammation is the main inducement of vascular disease, microRNA (miRNA) can influence inflammation in various ways, and Se deficiency can affect miRNAs expression. To study the mechanism of aorta damage caused by Se deficiency, we constructed a Se deficiency porcine aorta model and found that Se deficiency can significantly inhibit miR-223, which downregulates the expression of nucleotide-binding oligomerization domain-like receptor family 3 (NLRP3). Subsequently, we found that in Se deficiency group, NLRP3, and its downstream (caspase-1, apoptosis-related spot-like protein [ASC], IL-18, IL-1β) expression was significantly increased. In vitro, we cultured pig iliac endothelium cell lines, and constructed miR-223 knockdown and overexpression models. NLRP3 messenger RNA and protein levels were significant increased in the knockdown group, and decreased in the overexpression group. The results of this study show that Se deficiency in porcine arteries can induce inflammation through miR-223/NLRP3.

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“…The concentration of free radicals is low under physiological conditions, which is important to cell signal regulation, metabolism, survival, and apoptosis [24,25]. However, a large number of free radicals are induced when organisms are stimulated by physical factors or exogenous chemical substances; free radicals can covalently bind to biomacromolecules and peroxidize biofilm lipids to produce various toxic effects [26], which can lead to the occurrence of many diseases such as myocardial infarction [27,28] and various cancers [29].…”

Section: Discussionmentioning

confidence: 99%

IGF1 Knockdown Hinders Myocardial Development through Energy Metabolism Dysfunction Caused by ROS-Dependent FOXO Activation in the Chicken Heart

Gong

Yang

Liu

et al. 2019

Oxidative Medicine and Cellular Longevity

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Insulin-like growth factor 1 (IGF1) is a multifunctional cellular regulatory factor that can regulate cell growth and development by mediating growth hormone stimulation. However, the mechanism of IGF1 dysfunction in cardiomyocyte development is seldom reported. To study this, we employed the models of IGF1 knockdown in chicken embryo in vivo and in cardiomyocytes in vitro. We detected the antioxidant capacity, PI3K/Akt pathway, energy metabolism-related genes, and myocardial development-related genes. Our results revealed that the low expression of IGF1 can significantly suppress the antioxidant capacity and increase the ROS (P<0.05) levels, activating the AMPK and PI3K pathway by inhibiting the expression of IRS1. We also found that myocardial energy metabolism is blocked through IGF1, GLUT, and IGFBP inhibition, further inducing myocardial developmental disorder by inhibiting Mesp1, GATA, Nkx2.5, and MyoD expression. Altogether, we conclude that low IGF1 expression can hinder myocardial development through the dysfunction of energy metabolism caused by ROS-dependent FOXO activation.

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Targeting the miR-122/PKM2 autophagy axis relieves arsenic stress

Cited by 93 publications

References 55 publications

Interactions between Autophagy, Proinflammatory Cytokines, and Apoptosis in Neuropathic Pain: Granulocyte Colony Stimulating Factor as a Multipotent Therapy in Rats with Chronic Constriction Injury

Interactions between Autophagy, Proinflammatory Cytokines, and Apoptosis in Neuropathic Pain: Granulocyte Colony Stimulating Factor as a Multipotent Therapy in Rats with Chronic Constriction Injury

MicroRNA‐223 triggers inflammation in porcine aorta by activating NLRP3 inflammasome under selenium deficiency

IGF1 Knockdown Hinders Myocardial Development through Energy Metabolism Dysfunction Caused by ROS-Dependent FOXO Activation in the Chicken Heart

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