Inhibition of microRNA‐199a‐5p ameliorates oxygen‐glucose deprivation/reoxygenation‐induced apoptosis and oxidative stress in HT22 neurons by targeting Brg1 to activate Nrf2/HO‐1 signalling

Li, Feng; Liang, Jing; Tong, Hua; Zhu, Shuai; Tang, Dongfang

doi:10.1111/1440-1681.13265

Cited by 22 publications

(11 citation statements)

References 48 publications

(90 reference statements)

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“…Overexpression of BRG1 increases the activity of neurons, weakens apoptosis, and reduces the production of ROS, thus producing a protective effect on oxygen-glucose deprivation/reoxygenation- (OGD/R-) induced injury [ 45 ]. Additionally, further evidence indicates that inhibition of miR-144-3p or miR-199a-5p can alleviate OGD/R-induced neuronal injury by upregulating BRG1 to activate Nrf2/HO-1 signaling [ 46 , 47 ].…”

Section: Brg1 In Oxidative Stress Signalingmentioning

confidence: 99%

The Role of BRG1 in Antioxidant and Redox Signaling

You

Zhang

et al. 2020

Oxidative Medicine and Cellular Longevity

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Redox homeostasis is regulated by critical molecules that modulate antioxidant and redox signaling (ARS) within the cell. Imbalances among these molecules can lead to oxidative stress and damage to cell functions, causing a variety of diseases. Brahma-related gene 1 (BRG1), also known as SMARCA4, is the central ATPase catalytic subunit of the switch/sucrose nonfermentable (SWI/SNF) chromatin remodeling complex, which plays a core role in DNA replication, repair, recombination, and transcriptional regulation. Numerous recent studies show that BRG1 is involved in the regulation of various cellular processes associated with ARS. BRG1, as a major factor in chromatin remodeling, is essential for the repair of oxidative stress-induced DNA damage and the activation of antioxidant genes under oxidative stress. Consequently, a comprehensive understanding of the roles of BRG1 in redox homeostasis is crucial to understand the normal functioning as well as pathological mechanisms. In this review, we summarized and discussed the role of BRG1 in the regulation of ARS.

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Section: Brg1 In Oxidative Stress Signalingmentioning

confidence: 99%

The Role of BRG1 in Antioxidant and Redox Signaling

You

Zhang

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…In the muscle cells, hypoxamiRs downregulated by hypoxia involved ssc-miR-199a-5p controlling HIF1A expression 94 , a regulator of angiogenesis and mitochondrial antioxidants (ssc-miR-17-3p) 95 and two miRNAs regulating autophagy and apoptosis (ssc-miR-145-5p and ssc-miR-188-5p) 96 – 99 . Suppression of miR-199a-5p protects against H-R stress in mammalian heart and brain cells 100 – 103 , attenuates apoptosis 104 , 105 ), and contributes to higher aerobic capacity and tolerance to high-altitude hypoxia in humans 106 . Previous studies have associated lower levels of ssc-miR-17-3p with elevated mitochondrial enzyme activities in human colorectal cancer cells 95 , 107 .…”

Section: Discussionmentioning

confidence: 99%

Effects of hypoxia and reoxygenation on mitochondrial functions and transcriptional profiles of isolated brain and muscle porcine cells

Adzigbli

Sokolov

Wimmers

et al. 2022

Sci Rep

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Oxygen fluctuations might occur in mammalian tissues under physiological (e.g. at high altitudes) or pathological (e.g. ischemia–reperfusion) conditions. Mitochondria are the key target and potential amplifiers of hypoxia-reoxygenation (H-R) stress. Understanding the mitochondrial responses to H-R stress is important for identifying adaptive mechanisms and potential therapeutic solutions for pathologies associated with oxygen fluctuations. We explored metabolic response to H-R stress in two tissue types (muscle and brain) with different degrees of hypoxia tolerance in a domestic pig Sus scrofa focusing on the cellular responses independent of the systemic regulatory mechanisms. Isolated cells from the skeletal muscle (masseter) and brain (thalamus) were exposed to acute short-term (15 min) hypoxia followed by reoxygenation. The mitochondrial oxygen consumption, reactive oxygen species (ROS) production rates and transcriptional profiles of hypoxia-responsive mRNA and miRNA were determined. Mitochondria of the porcine brain cells showed a decrease in the resting respiration and ATP synthesis capacity whereas the mitochondria from the muscle cells showed robust respiration and less susceptibility to H-R stress. ROS production was not affected by the short-term H-R stress in the brain or muscle cells. Transcriptionally, prolyl hydroxylase domain protein EGLN3 was upregulated during hypoxia and suppressed during reoxygenation in porcine muscle cells. The decline in EGLN3 mRNA during reoxygenation was accompanied by an upregulation of hypoxia-inducible factor subunit α (HIF1A) transcripts in the muscle cells. However, in the brain cells, HIF1A mRNA levels were suppressed during reoxygenation. Other functionally important transcripts and miRNAs involved in antioxidant response, apoptosis, inflammation, and substrate oxidation were also differentially expressed between the muscle and brain cells. Suppression of miRNA levels during acute intermittent hypoxia was stronger in the brain cells affecting ~ 55% of all studied miRNA transcripts than in the muscle cells (~ 25% of miRNA) signifying transcriptional derepression of the respective mRNA targets. Our study provides insights into the potential molecular and physiological mechanisms contributing to different hypoxia sensitivity of the studied tissues and can serve as a starting point to better understand the biological processes associated with hypoxia stress, e.g. during ischemia and reperfusion.

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“…transcription of a variety of antioxidant genes, including heme oxygenase (HO-1) and NAD (P) H:quinone oxidoreductase 1 (NQO1) (12). The activation of Nrf2/HO-1 signaling pathway by targeting Brg1 improved H/R-induced HT22 neuron cell apoptosis and oxidative stress (13). The results indicated that Nrf2/HO-1 plays an important role in the pathological process of CIRI.…”

Section: Dihydromyricetin Inhibits Oxidative Stress and Apoptosis In ...mentioning

confidence: 97%

Dihydromyricetin inhibits oxidative stress and apoptosis in oxygen and glucose deprivation/reoxygenation‑induced HT22 cells by activating the Nrf2/HO‑1 pathway

et al. 2021

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Cerebral ischemia-reperfusion injury (CIRI) refers to the phenomenon that ischemic injury of the brain leads to the injury of brain cells, which is further aggravated after the recovery of blood reperfusion. Dihydromyricetin (DHM) has an effective therapeutic effect on vascular diseases; however, its role in CIRI has not been investigated. The oxygen and glucose deprivation/reoxygenation (OGD/R) cell model was used on HT22 hippocampal neurons in mice, by oxygen and sugar deprivation. DHM was found to increase the cell viability of HT22 cells following OGD/R induction. The levels of malondialdehyde (MDA) decreased, superoxide dismutase (SOD) and glutathione (GSH) in the OGD/R-induced HT22 cells increased following DHM treatment, accompanied by the decreased protein expression levels of NOX2 and NOX4. DHM also inhibited cell apoptosis induced by OGD/R, and decreased the protein expression levels of Bax and caspase-3, and increased the expression levels of Bcl-2. Moreover, the expression levels of the NF-E2-related factor 2 (Nrf2)/heme oxygenase (HO-1) signaling pathway-associated proteins in OGD/R-induced HT22 were increased following DHM treatment, and the effect of DHM on oxidative stress and apoptosis was reversed after the addition of the Nrf2/HO-1 pathway inhibitor, brusatol. In conclusion, DHM inhibited oxidative stress and apoptosis in OGD/R-induced HT22 cells by activating the Nrf2/HO-1 signaling pathway.

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Inhibition of microRNA‐199a‐5p ameliorates oxygen‐glucose deprivation/reoxygenation‐induced apoptosis and oxidative stress in HT22 neurons by targeting Brg1 to activate Nrf2/HO‐1 signalling

Cited by 22 publications

References 48 publications

The Role of BRG1 in Antioxidant and Redox Signaling

The Role of BRG1 in Antioxidant and Redox Signaling

Effects of hypoxia and reoxygenation on mitochondrial functions and transcriptional profiles of isolated brain and muscle porcine cells

Dihydromyricetin inhibits oxidative stress and apoptosis in oxygen and glucose deprivation/reoxygenation‑induced HT22 cells by activating the Nrf2/HO‑1 pathway

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